pituitrin and Acute-Disease

This is a literature review of the use of aquaretic in patients with acute decompensated heart failure (ADHF), including the physiologic function of vasopressin and its mechanism of action in heart failure patients, and aquaretic drugs with their respective risks and benefits.Vasopressin is one of several hormones that can cause hyponatremia and worsen congestion in ADHF patients. Aquaretics are a class of drugs that have an antagonistic effect on vasopressin receptors, especially V2R. Aquaretics use in ADHF patients can provide relief for congestive symptoms with no serious adverse effects. In-depth additional understanding regarding aquaretics may be useful for clinical judgments in treating ADHF patients.

Topics: Acute Disease; Heart Failure; Humans; Receptors, Vasopressin; Vasopressins

Hyponatremia is a common water balance disorder that often poses a diagnostic or therapeutic challenge. Therefore, guidelines were developed by professional organizations, one from within the United States (2013) and one from within Europe (2014). This review discusses the diagnosis and treatment of hyponatremia, comparing the two guidelines and highlighting recent developments. Diagnostically, the initial step is to differentiate hypotonic from nonhypotonic hyponatremia. Hypotonic hyponatremia is further differentiated on the basis of urine osmolality, urine sodium level, and volume status. Recently identified parameters, including fractional uric acid excretion and plasma copeptin concentration, may further improve the diagnostic approach. The treatment for hyponatremia is chosen on the basis of duration and symptoms. For acute or severely symptomatic hyponatremia, both guidelines adopted the approach of giving a bolus of hypertonic saline. Although fluid restriction remains the first-line treatment for most forms of chronic hyponatremia, therapy to increase renal free water excretion is often necessary. Vasopressin receptor antagonists, urea, and loop diuretics serve this purpose, but received different recommendations in the two guidelines. Such discrepancies may relate to different interpretations of the limited evidence or differences in guideline methodology. Nevertheless, the development of guidelines has been important in advancing this evolving field.

Topics: Acute Disease; Algorithms; Chronic Disease; Diagnosis, Differential; Glycopeptides; Humans; Hyponatremia; Practice Guidelines as Topic; Vasopressins

Hyponatremia is the most frequent electrolyte abnormality seen postoperatively in pediatric patients receiving maintenance fluid therapy. Hyponatremia is also common in acute pediatric illness. The main factors contributing to hyponatremia in these conditions are increased secretion of antidiuretic hormone (ADH) and routine use of sodium hypotonic fluids. An increased ADH secretion results in an impaired ability to excrete free water. If the sodium concentration falls to less than 125 mmol/L hyponatremic encephalopathy might develop, resulting in cerebral edema. This is avoided if hypotonic maintenance fluids are not used perioperatively or for rehydration or maintenance during acute critical illness in children.

Topics: Acute Disease; Child; Critical Illness; Fluid Therapy; Humans; Hyponatremia; Perioperative Care; Postoperative Complications; Practice Guidelines as Topic; Vasopressins

Hypopituitarism refers to deficiency of one or more hormones produced by the anterior pituitary or released from the posterior pituitary. Hypopituitarism is associated with excess mortality, a key risk factor being cortisol deficiency due to adrenocorticotropic hormone (ACTH) deficiency. Onset can be acute or insidious, and the most common cause in adulthood is a pituitary adenoma, or treatment with pituitary surgery or radiotherapy. Hypopituitarism is diagnosed based on baseline blood sampling for thyroid stimulating hormone, gonadotropin, and prolactin deficiencies, whereas for ACTH, growth hormone, and antidiuretic hormone deficiency dynamic stimulation tests are usually needed. Repeated pituitary function assessment at regular intervals is needed for diagnosis of the predictable but slowly evolving forms of hypopituitarism. Replacement treatment exists in the form of thyroxine, hydrocortisone, sex steroids, growth hormone, and desmopressin. If onset is acute, cortisol deficiency should be replaced first. Modifications in replacement treatment are needed during the transition from paediatric to adult endocrine care, and during pregnancy.

Topics: Acute Disease; Adenoma; Adrenocorticotropic Hormone; Chronic Disease; Deamino Arginine Vasopressin; Gonadal Steroid Hormones; Gonadotropins, Pituitary; Hormone Replacement Therapy; Human Growth Hormone; Humans; Hydrocortisone; Hypophysectomy; Hypopituitarism; Pituitary Gland; Pituitary Hormones, Anterior; Pituitary Irradiation; Pituitary Neoplasms; Prolactin; Radiotherapy; Thyrotropin; Thyroxine; Vasopressins

Acute decompensated heart failure (ADHF) is associated with substantial morbidity and mortality, and represents a considerable financial burden to society. Historically, few prospective, randomized, double-blinded trials have investigated the optimal management of ADHF, and most guideline recommendations are based primarily on expert opinion. However, in the last decade, a considerable amount of research has added to the understanding of the management of ADHF in both patients with fluid overload and low cardiac output. In addition, as mechanical circulatory support devices and heart transplantation continue to evolve, significant advances have also been made with regard to the proper selection of patients for advanced surgical options. Finally, several novel pharmacologic agents have shown promise in early trials and may represent the next steps in ADHF management. Although advances have been made over the past decade, many questions remain.

Topics: Acute Disease; Diuretics; Dopamine; Heart Failure; Heart Transplantation; Humans; Natriuretic Peptide, Brain; Nitroprusside; Ultrafiltration; Vasodilator Agents; Vasopressins

Acute variceal bleeding is a potentially life-threatening complication of portal hypertension. Management consists of emergent hemostasis, therapy directed at hemodynamic resuscitation, protection of the airway, and prevention and treatment of complications including prophylactic use of antibiotics. Endoscopic treatment remains the mainstay in the management of acute variceal bleeding in combination with pharmacotherapy aimed at reducing portal pressure. This article intends to highlight only the current nonendoscopic treatment approaches for control of acute variceal bleeding.

Topics: Acute Disease; Acute Kidney Injury; Anti-Bacterial Agents; Balloon Occlusion; Blood Transfusion; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hepatic Encephalopathy; Hormones; Humans; Hypertension, Portal; Intubation, Intratracheal; Liver Cirrhosis; Portasystemic Shunt, Transjugular Intrahepatic; Somatostatin; Vasoconstrictor Agents; Vasopressins

Most patients with heart failure (HF) already have or develop renal dysfunction; this might contribute to their poor outcome. Current treatment for HF can also contribute to worsen renal function. High furosemide doses are traditionally associated with worsening renal function (WRF), but patients with fluid overload may benefit of aggressive fluid removal. Unfortunately, promising therapies like vasopressin antagonists and adenosine antagonists have not been demonstrated to improve outcomes. Likewise, correction of low renal blood flow through dopamine, inotropic agents, or vasodilators does not seem to be associated with a clear benefit. However, transient WRF associated with acute HF treatment may not necessarily portend a poor prognosis. In this review, we focus on the strategies to detect renal dysfunction in acute HF, the underlying pathophysiological mechanisms, and the potential treatments.

Topics: Acute Disease; Adenosine; Biomarkers; Cardiotonic Agents; Diuretics; Dopamine; Heart Failure; Humans; Kidney; Kidney Diseases; Mineralocorticoid Receptor Antagonists; Prognosis; Vasodilator Agents; Vasopressins

Current treatment of acute decompensated heart failure (ADHF) has not reduced the significant morbidity or mortality associated with this disease, and has promoted drug development aimed at neurohormonal targets. Hypervolemic hyponatremia, which is linked to the nonosmotic release of arginine vasopressin, is associated with a poor prognosis in patients with heart failure (HF). Vasopressin acts on V(2) and V(1a) receptors to cause water retention and vasoconstriction, respectively. Clinical trials have demonstrated that vasopressin receptor antagonists (VRAs) are effective in treating hypervolemic hyponatremia in ADHF without a negative impact on renal function. The small hemodynamic benefit seen with VRA use appeared to result from V(2)-receptor antagonist-induced increase in urine output rather than from a vasodilatory drug effect. VRA use in ADHF trials was associated with minimal symptomatic improvement and no impact on morbidity or mortality. At present, clinical trial evidence does not support the routine use of VRAs in ADHF. Given the favorable renal profile of VRAs, studies on the possible benefit of VRAs in ADHF patients with renal insufficiency and diuretic resistance appear warranted.

Topics: Acute Disease; Animals; Antidiuretic Hormone Receptor Antagonists; Benzamides; Benzazepines; Clinical Trials as Topic; Heart Failure; Hemodynamics; Humans; Hyponatremia; Prognosis; Pyrroles; Tolvaptan; Vasoconstriction; Vasopressins

The acute acclimatization to high altitude is underpinned by a diuresis (and to a lesser extent a natriuresis) that facilitates a reduction in plasma volume. This allows a haemoconcentration to occur that increases the oxygen carrying capacity of a given volume of blood, a vital effect in the presence of a reduced partial pressure of oxygen. This critical acclimatization process is orchestrated by the endocrine system. This review will present the key evidence regarding the changes in several important hormones that affect this process.

Topics: Acclimatization; Acute Disease; Altitude Sickness; Atrial Natriuretic Factor; Diuresis; Hormones; Humans; Hydrocortisone; Mountaineering; Natriuretic Peptide, Brain; Plasma Volume; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Balance

Acute heart failure (AHF) is a frequent medical condition associated with a poor prognosis. Based on systolic blood pressure at presentation, patients with AHF can be classified into 5 clinical profiles enabling a more targeted use of standard medications including diuretics, vasodilators and inotropes. The most recent guidelines underline the importance of a rapid management and the favorable impact of heart failure programs, which reduce morbidity and mortality after an admission for AHF. New therapeutic perspectives include ultrafiltration, vasopressin and adenosine antagonists, relaxin and new inotropes such as istaroxime.

Topics: Acute Disease; Adenosine; Algorithms; Cardiotonic Agents; Diuretics; Drug Therapy, Combination; Etiocholanolone; Heart Failure; Hemodiafiltration; Humans; Oxygen Inhalation Therapy; Practice Guidelines as Topic; Prognosis; Relaxin; Risk Factors; Treatment Outcome; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

It is well established that endolymphatic hydrops plays a role in Ménière disease, even though the precise role is not fully understood and the presence of hydrops in the ear does not always result in symptoms of the disease. It nevertheless follows that a scientific understanding of how hydrops arises, how it affects the function of the ear, and how it can be manipulated or reversed could contribute to the development of effective treatments for the disease. Measurements in animal models in which endolymphatic hydrops has been induced have given numerous insights into the relationships between hydrops and other pathologic and electrophysiological changes, and how these changes influence the function of the ear. The prominent role of the endolymphatic sac in endolymph volume regulation, and the cascade of histopathological and electrophysiological changes that are associated with chronic endolymphatic hydrops, have now been established. An increasing number of models are now available that allow specific aspects of the interrelationships to be studied. The yclical nature of Ménière symptoms gives hope that treatments can be developed to maintain the ear in permanent state of remission, possibly by controlling endolymphatic hydrops, thereby avoiding the rogressive damage and secondary pathologic changes that may also contribute to the patient's symptoms.

Topics: Acute Disease; Aldosterone; Animals; Chronic Disease; Cyclic AMP; Disease Models, Animal; Endolymph; Endolymphatic Hydrops; Endolymphatic Sac; Hearing Loss; Humans; Intracranial Pressure; Ion Transport; Lipopolysaccharides; Magnetic Resonance Imaging; Noise; Vasopressins

Adaptive immunocompetence is maintained by growth hormone (GH), prolactin (PRL), and vasopressin (VP). Innate or natural immunocompetence depends on cytokines, hormones (especially of the hypothalamus-pituitary-adrenal axis), and catecholamines. The acute phase response (APR, or acute febrile illness) is an emergency defense reaction whereby the adaptive, T cell-dependent, immune reactions are suppressed and the innate immune function is dramatically amplified. Infection and various forms of injury induce APR. Cytokines [interleukin (IL)-1beta, tumor necrosis factor-alpha, and IL-6] stimulate corticotropin-releasing hormone (CRH) and VP secretion and cause a "sympathetic outflow." Colony-stimulating factors activate leukocytes. CRH is a powerful activator of the pituitary adrenocortical axis and elevates glucocorticoid (GC) levels. Cytokines, GCs, and catecholamines play fundamental roles in the amplification of natural immune defense mechanisms. VP supports the APR at this stage. However, VP remains active and is elevated for a longer period than is CRH. VP, but not CRH, is elevated during chronic inflammatory diseases. VP controls adaptive immune function and stimulates adrenocorticotropic hormone (ACTH) and PRL secretion. PRL maintains the function of the thymus and of the T cell-dependent adaptive immune system. The ACTH-adrenal axis stimulates natural immunity and of suppressor/regulatory T cells, which suppress the adaptive immune system. VP also has a direct effect on lymphoid cells, the significance of which remains to be elucidated. It is suggested that VP regulates the process of recovery from acute illness.

Topics: Acute Disease; Animals; Humans; Immune System; Immunocompetence; Neurosecretory Systems; Vasopressins; Wound Healing

Although most cases of acute gastrointestinal (GI) hemorrhage either spontaneously resolve or respond to medical management and/or endoscopic treatment, there remain a significant number of patients who require emergency evaluation and treatment by the interventional radiologist. Any angiographic evaluation should begin with selective catheterization of the artery supplying the most likely site of bleeding, as determined by the available clinical, endoscopic, and imaging data. If a source of hemorrhage is identified, superselective catheterization followed by transcatheter embolization with microcoils is the most effective means of successfully controlling hemorrhage while minimizing potential complications. This is now well-recognized as a viable and safe alternative to emergency surgery. In selected situations transcatheter intra-arterial infusion of vasopressin may also be useful in controlling acute GI bleeding. One must be aware of the various side effects and potential complications associated with this treatment, however, and recognize the high rebleeding rate. In this article, we review the current role of angiography, transcatheter arterial embolization, and infusion therapy in the evaluation and management of GI hemorrhage.

Topics: Acute Disease; Angiography, Digital Subtraction; Embolization, Therapeutic; Emergency Treatment; Gastrointestinal Hemorrhage; Hemostatic Techniques; Hemostatics; Humans; Infusions, Intra-Arterial; Predictive Value of Tests; Radiography, Interventional; Recurrence; Tomography, X-Ray Computed; Treatment Outcome; Vasopressins

Hyponatremia is the most common electrolyte disorder present in hospitalized patients. Acute and severe hyponatremia can cause significant morbidity and mortality. The present review discusses the epidemiology, causes, and a practical approach to the diagnosis and management of acute and chronic hyponatremia, including the appropriate use of hypertonic saline and potential future use of the new V2 vasopressin receptor antagonists in critically ill patients.. The increasing knowledge of aquaporin water channels and the role of vasopressin in water homeostasis have enhanced our understanding of hyponatremic disorders. Increased vasopressin secretion due to nonosmotic stimuli leads to decreased electrolyte-free water excretion with resulting water retention and hyponatremia. Vasopressin receptor antagonists induce electrolyte-free water diuresis without natriuresis and kaliuresis. Phase three trials indicate that these agents predictably reduce urine osmolality, increase electrolyte-free water excretion, and raise serum sodium concentration. They are likely to become a mainstay of treatment of euvolemic and hypervolemic hyponatremia.. The correct diagnosis and management of hyponatremia is complex and requires a systematic approach. Vasopressin receptor antagonists are potential tools in the management of hyponatremia. Further studies are needed to determine their role in the treatment of acute, severe, life-threatening hyponatremia as well as chronic hyponatremia.

Topics: Acute Disease; Humans; Hyponatremia; Osmolar Concentration; Osmotic Pressure; Receptors, Vasopressin; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

The majority of patients with acute decompensated heart failure are admitted with symptoms of congestion. The classic symptoms of "congestive" heart failure reflect fluid overload, that is, orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema; these symptoms can be so dramatic that it is not surprising that patients seek hospitalization. Activation of the renin angiotensin system coupled with sympathetic hyperactivity results in marked sodium retention and high filling pressures that ultimately bring about these congestive symptoms. The treatment goal of patients hospitalized with volume overload and high filling pressures is to improve symptoms by normalizing the filling pressure and volume status without worsening renal function. The current use of diuretics, vasodilators, and ultrafiltration, as well as potential future use of investigational agents such as oral vasopressin antagonists and adenosine A1-receptor antagonists, is surrounded by the important issues of when to stop intravenous therapy in hospitalized patients and the exact mechanism by which the filling pressures are normalized. New data from evidence-based clinical trials and optimal strategies for monitoring fluid overload will help define this issue and ultimately reduce mortality in these patients.

Topics: Acute Disease; Adenosine A1 Receptor Antagonists; Diuretics; Evidence-Based Medicine; Heart Failure; Hospitals; Humans; Medication Therapy Management; Patient Care Management; Practice Guidelines as Topic; Renin-Angiotensin System; Ultrafiltration; Vasodilator Agents; Vasopressins

Heart failure is one of the leading causes of hospitalizations in the United States. Concomitant and significant renal dysfunction is common in patients with heart failure. Increasingly, the syndrome of heart failure is one of cardiorenal failure, in which concomitant cardiac and renal dysfunctions exist, with each accelerating the progression of the other. One fourth of patients hospitalized for the treatment of acute decompensated heart failure will experience significant worsening of renal function, which is associated with worse outcomes. It remains unclear whether worsening renal function specifically contributes to poor outcomes or whether it is merely a marker of advanced cardiac and renal dysfunction. Diuretic resistance, with or without worsening renal function, is also common in acute decompensated heart failure, although the definition of diuretic resistance, its prevalence, and prognostic implications are less well defined. The term cardiorenal syndrome has been variably associated with cardiorenal failure, worsening renal function, and diuretic resistance but is more comprehensively defined as a state of advanced cardiorenal dysregulation manifest by one or all of these specific features. The pathophysiology of the cardiorenal syndrome is poorly understood and likely involves interrelated hemodynamic and neurohormonal mechanisms. When conventional therapy for acute decompensated heart failure fails, mechanical fluid removal via ultrafiltration, hemofiltration, or hemodialysis may be needed for refractory volume overload. While ultrafiltration can address diuretic resistance, whether ultrafiltration prevents worsening renal function or improves outcomes in patients with cardiorenal syndrome remains unclear. Evidence regarding the potential renal-preserving effects of nesiritide is mixed, and further studies on the efficacy and safety of different doses of nesiritide in heart failure therapy are warranted. Newer therapeutic agents, including vasopressin antagonists and adenosine antagonists, hold promise for the future, and clinical trials of these agents are underway.

Topics: Acute Disease; Adenosine; Cardiotonic Agents; Dopamine; Heart Failure; Humans; Natriuretic Agents; Natriuretic Peptide, Brain; Renal Insufficiency; Risk Factors; Sodium Potassium Chloride Symporter Inhibitors; Ultrafiltration; Vasopressins

Variceal bleeding is one of the most severe complications of portal hypertension related to liver cirrhosis. Primary prophylaxis is considered mandatory in patients with cirrhosis and high-risk oesophageal varices, and once varices have bled, every effort should be made to arrest the haemorrhage and prevent further bleeding episodes. In acute variceal bleeding, vasoactive drugs that lower portal pressure should be started even before endoscopy, and should be maintained for up to 5 days. The choice of vasoactive drug should be made according to local resources. Terlipressin, somatostatin and octreotide can be used; vasopressin plus transdermal nitroglycerin may be used if no other drug is available. In variceal bleeding, antibiotic therapy is also mandatory. In primary and secondary prophylaxis, beta-blockers are the mainstay of therapy. In secondary prophylaxis (but not in primary prophylaxis) these drugs can be combined with organic nitrates.

Topics: Acute Disease; Adrenergic beta-Antagonists; Antibiotic Prophylaxis; Drug Therapy, Combination; Esophageal and Gastric Varices; Humans; Hypertension, Portal; Liver Cirrhosis; Lypressin; Octreotide; Somatostatin; Terlipressin; Vasoconstrictor Agents; Vasopressins

Topics: Acute Disease; Anti-Anxiety Agents; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atropine; Cardiac Pacing, Artificial; Dopamine; Drug Overdose; Fluid Therapy; Humans; Hypertension; Hypotension; Isoproterenol; Nitroglycerin; Poisoning; Practice Guidelines as Topic; Propranolol; Vasopressins

Critical illness is characterized by striking alterations in the hypothalamic-anterior-pituitary-peripheral-hormone axes, the severity of which is associated with a high risk of morbidity and mortality. Most attempts to correct hormone balance have been shown ineffective or even harmful because of a lack of pathophysiologic insight. There is a biphasic (neuro)endocrine response to critical illness. The acute phase is characterized by an actively secreting pituitary, but the concentrations of most peripheral effector hormones are low, partly due to the development of target-organ resistance. In contrast, in prolonged critical illness, uniform (predominantly hypothalamic) suppression of the (neuro)endocrine axes contributes to the low serum levels of the respective target-organ hormones. The adaptations in the acute phase are considered to be beneficial for short-term survival. In the chronic phase, however, the observed (neuro)endocrine alterations appear to contribute to the general wasting syndrome. With the exception of intensive insulin therapy, and perhaps hydrocortisone administration for a subgroup of patients, no hormonal intervention has proven to beneficially affect outcome. The combined administration of hypothalamic releasing factors does, however, hold promise as a safe therapy to reverse the (neuro)endocrine and metabolic abnormalities of prolonged critical illness by concomitant reactivation of the different anterior-pituitary axes.

Topics: Acute Disease; Adrenal Glands; Catecholamines; Chronic Disease; Critical Illness; Endocrine System; Gonads; Hormones; Models, Biological; Thyroid Gland; Vasopressins

Vasopressin antagonists are a class of neurohormonal antagonists with applications in both the short-term and long-term management of patients with acute decompensated heart failure (ADHF). The pharmacologic effects of vasopressin antagonists include changes in fluid balance and hemodynamics that may improve symptoms and outcomes in patients hospitalized with ADHF. With chronic therapy, vasopressin antagonists offer the potential to improve outcomes through a variety of mechanisms, including more effective treatment of congestion, preservation or improvement of renal function, or a reduction in the use of concomitant loop diuretic therapy. Several vasopressin antagonists are currently in advanced clinical trials for the treatment of ADHF, chronic stable heart failure, and hyponatremia.

Topics: Acute Disease; Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Heart Failure; Humans; Pyrroles; Stroke Volume; Tolvaptan; Treatment Outcome; Vasoconstriction; Vasopressins

Acute decompensated heart failure represents a major, growing health problem in the developed world. However, until recently, relatively little research has been performed in this field to provide a basis for rational treatment strategies. The purpose of this review is to discuss the current approach and the potential future strategies for treatment of patients with acute decompensated heart failure.. Recent data have confirmed the heterogeneous nature of patients admitted with acute decompensated heart failure, and the limitations of the current therapeutic regimens with diuretics, intravenous vasodilators (ie, nitroglycerin, nitroprusside), and intravenous inotropes (ie, dobutamine, milrinone). A new vasodilator, nesiritide, has been demonstrated to improve hemodynamics and symptoms at 3 hours compared with nitroglycerin, and has been added to the therapeutic armamentarium in the United States. However, none of these agents has been shown to influence patient outcomes favorably. Given the high readmission rates, morbidity, and mortality of acute decompensated heart failure, other newer approaches, such as antagonists to a number of neurohumoral targets (ie, endothelin [tezosentan], vasopressin [conivaptan, tolvaptan], and adenosine) and non-cAMP-mediated inotropy (ie, levosimendan), are currently under investigation and showing promise.. Acute decompensated heart failure presents a challenging therapeutic problem for clinicians. Although they readily correct the hemodynamic abnormalities, current treatment strategies have significant limitations and have not been shown to improve morbidity or mortality. A number of new agents are under investigation with the goal of improving patient outcomes.

Topics: Acute Disease; Adenosine; Cardiotonic Agents; Catheterization, Swan-Ganz; Dobutamine; Drug Therapy; Endothelins; Forecasting; Heart Failure; Humans; Milrinone; Natriuretic Peptide, Brain; Vasopressins

In 85% of patients, renal colic is caused by renal-ureteral stones with extrinsic obstructions such as pelvic, retroperitoneal or intestinal abnormalities, and intrinsic reno-ureteral obstructions, e.g. junction pathologies and malformation, accounting for only 10 and 5%, respectively. The objectives of therapy for renal colic therapy are to eliminate pain, preserve renal function and eliminate the obstruction by the excretory pathway. Many drugs can be used to relieve pain: non-steroid anti-inflammatory agents (NSAIDs), opioid analgesics, antidiuretic hormone (ADH), loco-regional anesthesia and acupuncture. Opiates are the first-choice therapy during pregnancy as no other drug is indicated because of tetragenic potential. Paracetamol (N-acetyl-p-aminophenol) is the only NSAID that is registered for pediatric use because it has none of the adverse side effects that are associated with NSAIDs. Tamsulosin, an alpha-lithic drug, has very recently been included among the drugs that are used for stone expulsion. The rationale underlying its use is that a high concentration of alpha-1D adrenergic receptors has been recently detected in the terminal ureter, especially in the intramural tract. Inhibition of alpha-1D receptor stimulation should relax smooth muscle in the intramural ureteral tract, making stone expulsion easier.

Topics: Acute Disease; Analgesics, Opioid; Anti-Inflammatory Agents, Non-Steroidal; Female; Humans; Kidney Calculi; Male; Pain Measurement; Prognosis; Risk Assessment; Severity of Illness Index; Treatment Outcome; Ureteral Calculi; Vasopressins

Topics: Acute Disease; Esophageal and Gastric Varices; Esophageal Diseases; Gastrointestinal Hemorrhage; Humans; Lypressin; Rupture, Spontaneous; Somatostatin; Terlipressin; Vasoconstrictor Agents; Vasopressins

A POTENTIALLY SEVERE EVENT: Upper gastrointestinal haemorrhage in a cirrhotic patient is always extremely serious, particularly in the case of rupture of the oesophageal varices, which is the most frequent cause. THE TWO POLES OF TREATMENT: Early vasoactive treatment permits elastic ligature in optimal conditions using an endoscope. The prevention of other complications of cirrhosis is an essential element in the management of these patients.

Topics: Acute Disease; Emergencies; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemostasis, Endoscopic; Hemostatics; Hepatic Encephalopathy; Hormones; Humans; Hypertension, Portal; Ligation; Liver Cirrhosis; Octreotide; Recurrence; Risk Factors; Rupture; Sclerotherapy; Shock, Hemorrhagic; Somatostatin; Vasopressins

Emergency sclerotherapy is used as a first-line therapy for variceal bleeding in cirrhosis, although pharmacologic treatment stops bleeding in most patients. We performed a meta-analysis comparing emergency sclerotherapy with pharmacologic treatment.. MEDLINE (1968-2002), EMBASE (1986-2002), and the Cochrane Library (2002;4) were searched to retrieve randomized controlled trials comparing sclerotherapy with vasopressin (+/- nitroglycerin), terlipressin, somatostatin, or octreotide for variceal bleeding in cirrhosis. Outcome measures were failure to control bleeding, rebleeding, blood transfusions, adverse events, and mortality.. Fifteen trials were identified. Sclerotherapy was not superior to terlipressin, somatostatin, or octreotide for any outcome and to vasopressin for rebleeding, blood transfusions, death, and adverse events; it was superior to vasopressin for the control of bleeding in a single trial flawed by a potential detection bias. Sclerotherapy was associated with significantly more adverse events than somatostatin. In a predefined sensitivity analysis, combining all of the trials irrespective of the control treatment, risk differences (sclerotherapy minus control) and confidence intervals (CIs) were as follows: failure to control bleeding, -0.03 (-0.06 to 0.01); mortality, -0.035 (-0.07 to 0.008); adverse events, 0.08 (0.02 to 0.14). Mortality risk difference was -0.01 (-0.07 to 0.04) in good-quality trials and -0.08 (-0.14 to -0.02) in poor-quality trials.. Available evidence does not support emergency sclerotherapy as the first-line treatment of variceal bleeding in cirrhosis when compared with vasoactive drugs, which control bleeding in 83% of patients. Therefore, endoscopic therapy might be added only in pharmacologic treatment failures.

Topics: Acute Disease; Emergency Medical Services; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemostatics; Hormones; Humans; Liver Cirrhosis; Lypressin; Octreotide; Randomized Controlled Trials as Topic; Sclerotherapy; Somatostatin; Terlipressin; Vasoconstrictor Agents; Vasopressins

Variceal haemorrhage is a common medical emergency with a high mortality (30-50%). Adequate resuscitation is vital, and once stabilised the patient should be moved to a high-dependency area. Antibiotics reduce mortality, and the vasoactive drug terlipressin should be administered if early endoscopy is unavailable. Early endoscopy is essential both to make the diagnosis and to allow therapeutic measures to be performed. The evidence suggests that variceal band ligation is the most effective therapy for oesophageal varices. If gastric varices are found at the index endoscopy the evidence at present is inadequate to be certain which is the best treatment, but both endoscopic therapy with cyanoacrylate or thrombin and transjugular intrahepatic portosystemic stent shunt (TIPSS) have been reported to be of benefit. When initial treatments fail, rescue therapy should be initiated. Most authorities agree that TIPSS is the rescue therapy of choice. Many questions remain concerning the treatment of acute variceal bleeding, particularly the ideal therapy for gastric varices and the role of combination vasoactive and endoscopic therapy. Randomised controlled trials are required to answer these important issues.

Topics: Acute Disease; Catheterization; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemostatics; Hormones; Humans; Ligation; Lypressin; Octreotide; Portasystemic Shunt, Surgical; Randomized Controlled Trials as Topic; Recurrence; Sclerotherapy; Somatostatin; Terlipressin; Vasoconstrictor Agents; Vasopressins

The treatment of arterial gastrointestinal hemorrhage continues to evolve. Currently, most interventional radiologists approach bleeding both in the upper and lower gastrointestinal tract with intention to treat. Embolization has replaced local vasoconstrictive therapy as the catheter-based treatment of choice in many hospitals. Coaxial microcatheters have simplified embolotherapy and enabled lower gastrointestinal bleeding to be treated safely and effectively.

Topics: Acute Disease; Embolization, Therapeutic; Female; Gastrointestinal Hemorrhage; Hemostasis, Endoscopic; Hemostatics; Humans; Male; Mesenteric Arteries; Radiography; Vasopressins

Studies of octreotide have not demonstrated a consistent benefit in efficacy or safety compared with conventional therapies. This study statistically pooled existing trials to evaluate the safety and efficacy of octreotide for esophageal variceal hemorrhage.. We identified randomized trials of octreotide for variceal hemorrhage from computerized databases, scientific meeting abstracts, and the manufacturer of octreotide. Blinded reviewers abstracted the data, and a meta-analysis was performed.. Octreotide improved control of esophageal variceal hemorrhage compared with all alternative therapies combined (relative risk [RR], 0.63; 95% confidence interval [CI], 0.51-0.77); vasopressin/terlipressin (RR, 0.58; 95% CI, 0.42-0.81); or no additional intervention/placebo (among patients that received initial sclerotherapy/banding before randomization) (RR, 0.46; 95% CI, 0.32-0.67). Octreotide had comparable efficacy to immediate sclerotherapy for control of bleeding (RR, 0.94; 95% CI, 0.55-1.62), fewer major complications than vasopressin/terlipessin (RR, 0.31; 95% CI, 0.11-0.87), and a complication profile comparable to no intervention/placebo (RR, 1.06; 95% CI, 0.72-1.55). No specific alternative therapy demonstrated a mortality benefit.. These results favor octreotide over vasopressin/terlipressin in the control of esophageal variceal bleeding and suggest it is a safe and effective adjunctive therapy after variceal obliteration techniques. Trials are needed to determine the optimal dose, route, and duration of octreotide treatment.

Topics: Acute Disease; Esophageal and Gastric Varices; Hemorrhage; Hemostatics; Humans; Lypressin; Octreotide; Recurrence; Terlipressin; Vasopressins

Airway hemorrhage is a potentially rapidly fatal condition. Death may occur within minutes from asphyxiation before control can be achieved. The primary prognostic factors are the rate of bleeding and the underlying cardiopulmonary status of the patient. Bronchoscopy is central in management, but the goals differ, depending on circumstances. In stable patients who have minimal hemoptysis, bronchoscopy can diagnose the cause specifically and be used as the primary treatment modality. In the setting of massive or life-threatening bleeding, bronchoscopy primarily is performed to maintain ventilation and to direct endobronchial blockade. Although flexible bronchoscopy is an acceptable mode initially, there should be no delay in performing rigid bronchoscopy when it becomes apparent that bleeding is too vigorous to permit [figure: see text] successful airway exploration with the smaller flexible instrument. Once isolation of bleeding has been achieved, the choice must be made between embolization, surgical resection, or both of these procedures.

Topics: Acute Disease; Bronchoscopy; Combined Modality Therapy; Embolization, Therapeutic; Epinephrine; Hemoptysis; Humans; Prognosis; Vasopressins

The risk of recurrent variceal bleeding after an acute episode of bleeding has been controlled in significant with rebleeding rates as high as 80% between one and two years. Pharmacologic therapy has a definite role in the prevention of recurrent variceal bleeding and should be started as soon as the acute bleeding event has been controlled. Serial hemodynamic measurements are critical for success. Non-selective beta-blocker therapy is a reasonable first line approach followed by the addition of a long-acting nitrate for patients not achieving a 20% reduction in the hepatic venous pressure gradient. Most patients will require combination pharmacotherapy or combined endoscopic therapy with pharmacotherapy.

Topics: Acute Disease; Antihypertensive Agents; Blood Flow Velocity; Drug Therapy, Combination; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hormones; Humans; Liver Circulation; Lypressin; Nitroglycerin; Portal Pressure; Risk Factors; Somatostatin; Terlipressin; Treatment Outcome; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Although sclerotherapy is the current standard therapy for bleeding esophageal varices, the best method for initial control is unclear. The aim of this meta-analysis was to compare the efficacy and toxicity of somatostatin and vasopressin in short-term treatment of hemorrhage from esophageal varices.. Using MEDLINE, all randomized trials comparing somatostatin with vasopressin in subjects with endoscopically documented acute esophageal variceal bleeding were identified. The quality of each study was critically and independently evaluated, and quantitative data for initial cessation of bleeding, sustained control of bleeding, and major adverse effects were abstracted. The relative risk (RR) and number needed to be treated were calculated.. The RR or likelihood of achieving initial control of bleeding with somatostatin vs. vasopressin was 1.62 (95% confidence interval [CI], 1.37-1.93), and the number needed to be treated was 3.7, i.e., between 3 and 4 patients would have to be treated with somatostatin for 1 patient to derive additional benefit over vasopressin. For trials that measured sustained control of bleeding, somatostatin was superior to vasopressin (RR, 1.28 [95% CI, 1.00-1.65]; number needed to be treated, 8.8). The risk of adverse effects was greater for subjects given vasopressin (10% vs. 0%; P = 0.00007).. This meta-analysis suggests that somatostatin is more efficacious in controlling acute hemorrhage from esophageal varices and has a lower risk of adverse effects than vasopressin.

Topics: Acute Disease; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemostatics; Humans; Research Design; Somatostatin; Treatment Outcome; Vasopressins

The endocrine response to stress is complex. Elevations in the serum concentrations of the "classic" stress hormones, epinephrine and cortisol, occur following many kinds of physiologic challenge and are accompanied by elevations in corticotropin, GH, and glucagon levels. These changes are probably responsible for the hyperglycemia and hypercatabolism common to most critical illness. If volume depletion is present, vasopressin, renin, and aldosterone secretion are also likely to be stimulated. These hormones, if present in excess, may produce fluid retention and hyponatremia. In some critically ill patients, there is a dissociation of renin and aldosterone production called hyperreninemic hypoaldosteronism, but the clinical importance of this syndrome is poorly understood. Thyroid hormone metabolism is commonly affected by critical illness, which results in characteristic abnormalities of thyroid function testing known as the euthyroid sick syndrome. The reproductive axis is exquisitely sensitive to physiologic stress; hypogonadotropic hypogonadism is a common finding in critical illness. The ongoing challenge to the clinician is to determine whether seemingly abnormal hormone measurements in critically ill patients reflect an appropriate homeostatic response to severe illness or, instead, whether they denote an independent metabolic disorder that might actually cause or contribute to the patient's unstable condition. In view of the exceedingly complex (and poorly understood) interactions involved in the human response to a severe illness, a thoughtful approach to the whole patient is essential and far preferable to indiscriminate hormone testing. Such testing, at best, may be uninterpretable in light of the clinical circumstances or, at worst, may lead to therapeutic misadventures.

Topics: Acute Disease; Catecholamines; Emergencies; Endocrine System Diseases; Glucagon; Glucocorticoids; Gonadal Steroid Hormones; Growth Hormone; Humans; Renin-Angiotensin System; Thyroid Hormones; Vasopressins

Topics: Acute Disease; Catheterization; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Liver Transplantation; Portasystemic Shunt, Surgical; Radiography; Rupture, Spontaneous; Sclerotherapy; Somatostatin; Vasopressins

In response to stressors, the central nervous system of livestock (and other mammalian species) evokes physiological responses that ultimately result in activation of the hypothalamo-pituitary-adrenocortical (HPA) axis and the sympatho-adrenal axis. The responses of these major systems are presumed to have adaptive and homeostatic value during periods of stress. The major hormone regulating the synthesis and secretion of adrenal glucocorticoids is ACTH. In sheep, cattle, and pigs, both corticotropin-releasing hormone (CRH) and vasopressin (VP) participate in the regulation of secretion of ACTH, and the two peptides seem to interact to enhance that secretion. In cattle and pigs, CRH is the more potent peptide, whereas VP is the more potent in sheep. In addition to its better-known role in regulating pituitary function, CRH also may participate as a neurotransmitter acting centrally to enhance sympathetic activation of the adrenal medulla. Many experimental models of stress have been evaluated that reliably activate the HPA axis and the sympatho-adrenal medullary axis, and some of these model systems also reduce functions of cells of the immune system. Recent data support an important role of stressor-activation of the sympathetics rather than increased glucocorticoids per se in modulating some measures of immune function in response to stress. Thus, current dogma of glucocorticoids as the primary mediator of stressor-associated alteration in immune function of domestic livestock may require reevaluation.

Topics: Acute Disease; Adrenocorticotropic Hormone; Animals; Animals, Domestic; Corticotropin-Releasing Hormone; Disease Models, Animal; Hydrocortisone; Hypothalamo-Hypophyseal System; Immune System; Pituitary-Adrenal System; Restraint, Physical; Social Isolation; Stress, Physiological; Sympathetic Nervous System; Vasopressins

Clinically, the earlier acute vertiginous attacks in Menière's disease and the later deafness appear to constitute a continuum. It is therefore possible that effective treatment of the cause of the acute attacks might prevent the later auditory symptoms. This paper describes biochemical events preceding the acute attacks, and then points to a common factor in the acute and chronic states. If true, this occurrence supports use of intravenous calcium gluconate to abort or cut short an acute attack. Because of the complexities of the situation, it is probable that not every Menière's disease patient will respond to this treatment and a controlled widespread trial is necessary.

Topics: Acute Disease; Aldosterone; Animals; Humans; Hyaluronic Acid; Hyaluronoglucosaminidase; Meniere Disease; Vasopressins

Once the bleeding patient has been resuscitated and the diagnosis of acute variceal hemorrhage established by endoscopy, emergency injection sclerotherapy should be employed as the therapeutic option of choice. Endoscopic band ligation is a promising new technique that may prove to be as effective as sclerotherapy, with fewer complications. Pharmacologic treatment (with vasopressin and nitroglycerin) and balloon tamponade remain important alternative treatments, both as empiric temporizing therapy before sclerotherapy can be arranged and in the approximately 30% of patients who continue to bleed after a single sclerotherapy session. Continued bleeding in many of these patients can be controlled with a second session of sclerotherapy. If active acute bleeding persists after two sclerotherapy treatments, treatment should be considered a failure. Some of these patients may be suitable for surgical treatment with either staple-gun transection of the esophagus or emergency portacaval shunting.

Topics: Acute Disease; Balloon Occlusion; Catheterization; Drug Administration Schedule; Emergencies; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Ligation; Nitroglycerin; Portacaval Shunt, Surgical; Sclerotherapy; Somatostatin; Vasopressins

The goals of therapy in acute variceal bleeding are to arrest haemorrhage and to prevent deterioration of liver function and complications related to bleeding. The measures used to stop acute bleeding should, ideally, also prevent the very early rebleeding that is frequently seen with bleeding varices. Variceal bleeding should be managed by a gastrointestinal bleeding team with intensive nursing care. Diagnostic endoscopy is mandatory once initial resuscitation has been achieved, and allows immediate injection sclerotherapy of varices. Drug therapy can be used as the first treatment in patients admitted with variceal bleeding since it can be given immediately. Of the available drugs, somatostatin has the least side effects and is as effective as vasopressin, terlipressin and the combination of vasopressin and an organic nitrate vasodilator. The role of drugs needs to be studied in combination with sclerotherapy. Sclerotherapy remains the mainstay of management as it achieves the twin goals of stopping active bleeding and preventing early rebleeding. Injection of tissue adhesive and endoscopic ligation or 'banding' are new endoscopic techniques that have shown promise in preliminary trials and are currently being assessed more widely. Balloon tamponade is a temporary measure used to prevent exsanguination. Surgery should be reserved for those patients in whom sclerotherapy is unsuccessful or cannot be carried out. Oesophageal staple transection is the most used operation. The new interventional radiological technique of transjugular intrahepatic portosystemic shunting will probably replace surgery in the future, but its role in acute variceal bleeding has yet to be fully defined.

Topics: Acute Disease; Animals; Balloon Occlusion; Catheterization; Drug Therapy, Combination; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Lypressin; Nitroglycerin; Sclerotherapy; Somatostatin; Terlipressin; Vasopressins

Following the demonstration that somatostatin lowered portal pressure in cirrhotic patients with portal hypertension, 2 uncontrolled reports suggested that the hormone might be useful in the control of acute variceal haemorrhage. Subsequently, a number of randomised controlled trials have indicated that somatostatin may have an efficacy as good as or better than either vasopressin or combined vasopressin and nitroglycerin therapy and is associated with fewer side effects. Somatostatin has an efficacy comparable to balloon tamponade, histamine-2-receptor antagonists and injection sclerotherapy. One double-blind randomised controlled trial demonstrated a significant benefit of somatostatin over placebo in the control of variceal bleeding whereas a second did not show any significant difference between treatments. In all the controlled trials, the average control rate achieved with somatostatin administration was 69% and it was not associated with any major side effects. Somatostatin administration has also been shown in uncontrolled series to be very effective in controlling postinjection sclerotherapy bleeding from the varices per se, and from oesophageal ulcers and oesophagitis. Few data are available on the long acting analogue of somatostatin, octreotide, but preliminary data suggest that it may be as effective and safe as the native hormone in controlling the acute variceal bleeding and postinjection sclerotherapy haemorrhage. It is concluded that there may be a case for instituting somatostatin therapy as soon as the patient enters hospital to facilitate sclerotherapy, and for continuing treatment for 5 days after sclerotherapy when the risk of recurrent bleeding is highest.

Topics: Acute Disease; Balloon Occlusion; Catheterization; Combined Modality Therapy; Double-Blind Method; Drug Therapy, Combination; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Nitroglycerin; Octreotide; Sclerotherapy; Somatostatin; Vasopressins

The management of both acute and recurrent variceal bleeding continues to be a significant challenge to the clinician. The cause and pathogenesis of portal hypertension has been described. Alcoholic cirrhosis is the most common cause of intrahepatic sinusoidal and postsinusoidal obstruction in the United States. Long term survival depends on rapid institution of an established protocol of surgical management for variceal hemorrhage. A patient who presents with variceal bleeding must be rapidly stabilized with fluid resuscitation, and specific measures, such as the use of vasopressin and balloon tamponade, must be instituted to control hemorrhage so that endoscopy can be used to establish the diagnosis. Sclerotherapy achieves a high rate of success in the acute situation, but if hemorrhage cannot be controlled, percutaneous transhepatic embolization or emergent shunting must be performed, depending on the condition of the patient. Angiography, prior to surgical treatment, is necessary to define venous anatomy and determine portal hemodynamics, both of which provide information vital in choosing the type of shunt. If bleeding is massive and the patient is unstable, H-grafts are most appropriate, for they are technically easier and give excellent short term results. In a stable Child's A or B patient with minor ascites as well as suitable anatomy and hepatopedal flow, DSRS is the procedure of choice because it produces the smallest degree of HE postoperatively and increases the survival rate for nonalcoholics. If this is not feasible or if the surgeon lacks the technical expertise to perform DSRS, PCS is the logical alternative. In view of the data from the series observed in the United States, ablative procedures cannot be recommended at the present for the treatment of variceal bleeding. In the Child's C poor-risk patient, the operative mortality rate is prohibitive, and only nonsurgical means should be used to establish control of bleeding. In the elective situation, the surgical options change. The efficacy of ES as a definitive procedure to control recurrent variceal bleeding is unproved, and rebleeding can be significant; therefore, it cannot be recommended. H-grafts have a prohibitively high rate of long term thrombosis and are also not recommended, and the Linton or proximal splenorenal shunt offers no advantages over conventional portacaval shunting. Moreover, arterialization of the hepatic stumps of the portal vein does not prevent hepatic encephal

Topics: Acute Disease; Clinical Trials as Topic; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hepatic Encephalopathy; Humans; Hypertension, Portal; Liver Cirrhosis, Alcoholic; Portacaval Shunt, Surgical; Radiography; Recurrence; Sclerosing Solutions; Vasopressins

A male quadriplegic (C6--complete) with persistent chronic hyponatremia (serum sodium values ranging consistently from 117-132 mmol/L) developed acute hyponatremia with a serum sodium concentration of 98 mmol/L. This extreme hyponatremia related, in part, to a reversible defect in the excretion of a water load, while on a low (46 mmol/day) sodium diet. Subsequent ingestion of a normal sodium diet (150 mmol/day), with or without 0.1 mg of fludrocortisone (Florinef), reestablished his ability to excrete a water load normally. The etiology of this patient's hyponatremia is discussed as well as the unique concordance of factors which make hyponatremia a common occurrence among spinal-cord injured patients.

Topics: Acute Disease; Diet, Sodium-Restricted; Fludrocortisone; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Sodium, Dietary; Spinal Cord Injuries; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Acute Disease; Adrenergic beta-Antagonists; Animals; Drug Therapy, Combination; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Lypressin; Nitroglycerin; Nitroprusside; Recurrence; Risk; Somatostatin; Terlipressin; Vasopressins

Topics: Acute Disease; Endoscopy; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hypertension, Portal; Nadolol; Propranolol; Somatostatin; Vasopressins

Topics: Acute Disease; Adult; Cholestasis; Cystic Fibrosis; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Infant; Sclerosing Solutions; Splenomegaly; Vasopressins

In recent years the technique of selective portasystemic shunting (Warren procedure) and sclerotherapy, and also the possibility of lowering portal pressure with beta-blockers, have changed the approach to management of patients with bleeding esophageal varices. Treatment of these patients is reviewed in the light of experience of 204 cases and the literature. The advantages and disadvantages of vasopressin, balloon tamponade, sclerotherapy, transhepatic embolization and various shunt and non-shunt operations in the acute phase are presented. For elective cases the discussion centers mainly on treatment by distal splenorenal shunt and sclerotherapy.

Topics: Acute Disease; Clinical Trials as Topic; Embolization, Therapeutic; Emergencies; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Lypressin; Portasystemic Shunt, Surgical; Prospective Studies; Recurrence; Sclerosing Solutions; Terlipressin; Vasopressins

Somatostatin (SST) has been shown by several controlled studies to be effective in halting acute severe bleeding from ulcerative and erosive lesions of the upper intestinal tract. Its efficacy for the treatment of bleeding esophageal varices is less certain, and more controlled studies are necessary. Intravenous administration of SST or subcutaneous application of the new synthetic SST-analogues produces a decrease in serum hormone levels and abolition of symptoms in patients with endocrine-active tumors such as vipoma, glucagonoma and carcinoid. SST has no effect on the outcome of acute pancreatitis, and experience with SST in treating intestinal fistulas is very limited.

Topics: Acute Disease; Cimetidine; Clinical Trials as Topic; Double-Blind Method; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Intestinal Fistula; Pancreatic Fistula; Pancreatitis; Paraneoplastic Endocrine Syndromes; Peptic Ulcer Hemorrhage; Prospective Studies; Random Allocation; Ranitidine; Secretin; Somatostatin; Vasopressins

Bleeding from esophageal varices is a feared complication of liver cirrhosis with high mortality. Pharmacotherapy of the acute bleeding episode with vasopressin has been shown to be effective in controlled studies, but side effects of this therapy are high and therefore replacement of vasopressin with somatostatin is under investigation. Another potential lead is the combination of vasopressin with vasodilators such as nitroglycerin. While acute pharmacotherapy of the patient with esophageal varices is well accepted, chronic or prophylactic pharmacotherapy is still in the investigative stage. Prophylactic therapy with beta-blockers, e.g. propranolol, has been shown to be effective in compensated patients with alcoholic cirrhosis. In patients with more advanced stages of the disease, or with cirrhosis of other etiology, the effectiveness of propranolol has not been proven. The mechanism of propranolol is similar to that of vasopressin, i.e. it lowers portal pressure by reducing portal flow. To maintain function of the affected organ, an alternative approach--namely lowering of portal pressure through reduction of the pathologically elevated resistance--should be actively investigated.

Topics: Acute Disease; Adrenergic beta-Antagonists; Chronic Disease; Clinical Trials as Topic; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Propranolol; Random Allocation; Somatostatin; Vasopressins

The genesis of renovascular hypertension follows a continuum from an acute to a chronic phase. Reduction in renal perfusion initiates renin release and angiotensin-mediated systemic vasoconstriction. Aldosterone secretion, sodium and water retention, and expansion of the extracellular volume ensue. Sustained hypertension is further maintained by interacting physiologic mechanisms including increased angiotensin II sensitivity, vasopressin, ouabain-like substance, the sympathetic nervous system, CNS mechanisms, autoregulation, and structural changes.

Topics: Acute Disease; Angiotensin II; Animals; Arterial Occlusive Diseases; Central Nervous System; Chronic Disease; Disease Models, Animal; Dogs; Hemodynamics; Hypertension, Renovascular; Kidney; Ouabain; Perfusion; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Vasoconstriction; Vasopressins

The vasoconstrictor and vasopressor actions of vasopressin have been revealed in recent research through the use of highly specific and sensitive radioimmunoassays, employment of peptide antagonists, and comparison with an animal model which has hereditary absence of this hormone, the Brattleboro rat. Factors now known to modify the pressor effect of vasopressin are the baroreflexes, local vascular prostaglandin production, and a specific interaction with angiotensin II. In experimental models the volume retaining, but not the vasoconstrictor effect of vasopressin is necessary for mineralocorticoid-salt hypertension. Vasopressin contributes directly to the increase in arterial pressure of glycerol induced acute renal failure. In nephrectomized rats, plasma vasopressin is elevated and contributes directly to maintenance of pressure. Vasopressin antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension and in one genetic model, spontaneously hypertensive rat (SHR), but the peptide is not necessary for hypertension in these models. Plasma vasopressin is reduced in primary aldosteronism, but may be elevated in malignant hypertension. In essential hypertension, there is considerable disagreement among various studies in which plasma vasopressin, urine vasopressin excretion, platelet associated vasopressin, or vasopressin-neurophysin were measured as to whether there is evidence for increased secretion of vasopressin. Only preliminary studies of vasopressin antagonism in clinical hypertension have been reported. At present, there is no conclusive evidence that elevated vasopressin secretion occurs or is necessary for any form of clinical hypertension.

Topics: Acute Disease; Acute Kidney Injury; Animals; Central Nervous System Diseases; Desoxycorticosterone; Humans; Hypertension; Hypertension, Malignant; Hypertension, Renal; Hypertension, Renovascular; Kidney Failure, Chronic; Rats; Rats, Brattleboro; Rats, Inbred SHR; Vasopressins

Topics: Acute Disease; Embolization, Therapeutic; Esophageal and Gastric Varices; Esophagus; Gastrointestinal Hemorrhage; Hemostatic Techniques; Humans; Hypertension, Portal; Intubation; Intubation, Gastrointestinal; Liver Cirrhosis; Sclerosing Solutions; Vasopressins

Topics: Acute Disease; Arginine Vasopressin; Chronic Disease; Hyponatremia; Osmolar Concentration; Sodium Chloride; Urine; Vasopressins; Water; Water-Electrolyte Balance

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.

Topics: Acute Disease; Analgesics; Humans; Hypercalcemia; Immune System Diseases; Kidney Calculi; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubular Necrosis, Acute; Necrosis; Nephrosis; Nephrotic Syndrome; Potassium Deficiency; Proteins; Tetracyclines; Ureteral Diseases; Ureteral Obstruction; Urologic Neoplasms; Vascular Diseases; Vasopressins

Topics: Acute Disease; Animals; Duodenal Ulcer; Gastrectomy; Gastric Mucosa; Gastritis; Gastroscopy; Humans; Intestinal Mucosa; Peptic Ulcer; Peptic Ulcer Hemorrhage; Permeability; Stomach Ulcer; Stress, Psychological; Vagotomy; Vasopressins

Pneumonia is one of the most serious infections in the neonate and is responsible for a large percentage of neonatal mortality. Pneumonia in a premature or term infant who is debilitated by an underlying problem such as hyaline membrane disease carries an extremely high morbidity and mortality. Since most of the bacterial pneumonias are treatable, early recognition and diagnosis and vigorous treatment are essential. X-ray findings, though helpful, serve only as a guideline. Prognosis is adversely affected if pneumonia results in generalized sepsis, leading to meningitis, disseminated intravascular coagulation, and osteomyelitis. Prompt antibiotic treatment should be begun before the etiologic agent or drug susceptibility is known.

Topics: Acute Disease; Ampicillin; Bacterial Infections; Gentamicins; Humans; Infant, Newborn; Infant, Newborn, Diseases; Kanamycin; Penicillins; Pneumonia; Pneumonia, Aspiration; Pneumonia, Viral; Syphilis, Congenital; Tuberculosis, Pulmonary; Vasopressins

Ultrasonic examination of the pancreas is rendered difficult by the echogenic characteristics of the organ, by its depth, by the overlying gas, and by bony structures and anatomic variations. The reintroduction of gray-scale imaging promises to simplify the technique and expand its usefulness. The 75Se-/-selenomethionine scan is a reliable test when performed after effective pancreatic stimulation with a scintillation camera that permits the angulation required to separate pancreas from liver. Gallium-67-citrate may be important for both mapping inflammatory processes and imaging some tumors. Retrograde pancreatography has developed into a rather reliable and sensitive method of visualizing pancreatic duct abnormalities. Angiography remains the most reliable technique for finding small lesions, while computerized axial tomography appears a promising modality in the near future. In acute pancreatitis, gallium scanning may find a place alongside plain films, GI series, and echography. Chronic pancreatitis appears best studied by pancreatography, possibly with selenomethionine scanning as a function study and echography to find associated mass lesions. Pseudocysts are most easily located by ultrasound examination. Screening for pancreatic carcinoma is done most effectively with selenomethionine scanning when the index of suspicion is low and with pancreatography or arteriography when it is high. Echography is useful for localization for aspiration biopsy and for sequential evaluation of therapeutic response. Islet-cell tumors are best found by angiographic studies.

Topics: Acute Disease; Adenoma, Islet Cell; Adult; Female; Gallium Radioisotopes; Hormones, Ectopic; Humans; Male; Middle Aged; Pancreatic Cyst; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatitis; Paraneoplastic Endocrine Syndromes; Radionuclide Imaging; Selenomethionine; Ultrasonography; Vasopressins; Zollinger-Ellison Syndrome

Topics: Acute Disease; Alcoholic Intoxication; Autonomic Nervous System; Blood Pressure; Body Temperature; Cardiovascular System; Electrocardiography; Ethanol; Heart; Humans; Time Factors; Vasopressins

Topics: Acute Disease; Animals; Dogs; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Pituitary Hormones, Posterior; Tampons, Surgical; Vasopressins

Hospitalization for acute decompensated heart failure (ADHF) involves substantial morbidity and mortality. Current management strategies have major limitations, and there has been little progress in the development of newer therapies. Arginine vasopressin-receptor antagonists may have promise in the treatment of ADHF in view of their ability to facilitate diuresis. This pilot study was designed to evaluate the efficacy and safety of intravenous conivaptan, a dual arginine vasopressin V(1A)/V(2)-receptor antagonist, in treating ADHF.. In a double-blind, multicenter trial, 170 patients hospitalized for worsening heart failure and given standard therapy were randomly assigned to treatment with conivaptan (20-mg loading dose followed by 2 successive 24-hour continuous infusions of 40, 80, or 120 mg/d) or placebo. The conivaptan and placebo groups did not differ significantly in patient or clinician assessments of global and respiratory status at 48 hours. There was no evidence of worsening heart failure in any group. Conivaptan at each dosage increased urine output significantly more than placebo at 24 hours (P

Topics: Acute Disease; Aged; Antidiuretic Hormone Receptor Antagonists; Area Under Curve; Benzazepines; Disease Progression; Diuresis; Double-Blind Method; Female; Heart Failure; Humans; Male; Middle Aged; Pain Measurement; Pilot Projects; Receptors, Vasopressin; Vasopressins

Topics: Acute Disease; Double-Blind Method; Gastric Mucosa; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Liver Cirrhosis; Lypressin; Perfusion; Stomach Diseases; Terlipressin; Vasoconstrictor Agents; Vasopressins

Following the demonstration that somatostatin lowered portal pressure in cirrhotic patients with portal hypertension, 2 uncontrolled reports suggested that the hormone might be useful in the control of acute variceal haemorrhage. Subsequently, a number of randomised controlled trials have indicated that somatostatin may have an efficacy as good as or better than either vasopressin or combined vasopressin and nitroglycerin therapy and is associated with fewer side effects. Somatostatin has an efficacy comparable to balloon tamponade, histamine-2-receptor antagonists and injection sclerotherapy. One double-blind randomised controlled trial demonstrated a significant benefit of somatostatin over placebo in the control of variceal bleeding whereas a second did not show any significant difference between treatments. In all the controlled trials, the average control rate achieved with somatostatin administration was 69% and it was not associated with any major side effects. Somatostatin administration has also been shown in uncontrolled series to be very effective in controlling postinjection sclerotherapy bleeding from the varices per se, and from oesophageal ulcers and oesophagitis. Few data are available on the long acting analogue of somatostatin, octreotide, but preliminary data suggest that it may be as effective and safe as the native hormone in controlling the acute variceal bleeding and postinjection sclerotherapy haemorrhage. It is concluded that there may be a case for instituting somatostatin therapy as soon as the patient enters hospital to facilitate sclerotherapy, and for continuing treatment for 5 days after sclerotherapy when the risk of recurrent bleeding is highest.

Topics: Acute Disease; Balloon Occlusion; Catheterization; Combined Modality Therapy; Double-Blind Method; Drug Therapy, Combination; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Nitroglycerin; Octreotide; Sclerotherapy; Somatostatin; Vasopressins

Vasopressin infusion and esophageal tamponade are still widely used to arrest variceal bleeding, but no objective evidence exists on the superiority of either of the two procedures. In this study, 108 cirrhotic patients bleeding from varices were included in a prospective, randomized trial to investigate the comparative effectiveness and safety of balloon tamponade (using the Sengstaken-Blakemore tube for esophageal varices and the Linton-Nachlas tube for gastric varices) (n = 52) and intravenous vasopressin infusion (0.4 to 0.8 mu/min) plus intravenous nitroglycerin infusion (40 to 400 micrograms/min) (n = 56). Both treatments were maintained for 24-hr. The hemostatic efficacy according to the intention to treat was 86.5% for tamponade and 66% for pharmacological therapy (p less than 0.01). No significant differences were found with respect to rebleeding during the first 72 hr after treatment, mortality rate or side effects. These results suggest that esophageal tamponade is more effective than vasopressin/nitroglycerin infusion in the treatment of variceal bleeding in cirrhotic patients.

Topics: Acute Disease; Adult; Aged; Balloon Occlusion; Catheterization; Drug Therapy, Combination; Esophageal and Gastric Varices; Esophagus; Female; Humans; Infusions, Intravenous; Male; Middle Aged; Multivariate Analysis; Nitroglycerin; Vasopressins

The management of both acute and recurrent variceal bleeding continues to be a significant challenge to the clinician. The cause and pathogenesis of portal hypertension has been described. Alcoholic cirrhosis is the most common cause of intrahepatic sinusoidal and postsinusoidal obstruction in the United States. Long term survival depends on rapid institution of an established protocol of surgical management for variceal hemorrhage. A patient who presents with variceal bleeding must be rapidly stabilized with fluid resuscitation, and specific measures, such as the use of vasopressin and balloon tamponade, must be instituted to control hemorrhage so that endoscopy can be used to establish the diagnosis. Sclerotherapy achieves a high rate of success in the acute situation, but if hemorrhage cannot be controlled, percutaneous transhepatic embolization or emergent shunting must be performed, depending on the condition of the patient. Angiography, prior to surgical treatment, is necessary to define venous anatomy and determine portal hemodynamics, both of which provide information vital in choosing the type of shunt. If bleeding is massive and the patient is unstable, H-grafts are most appropriate, for they are technically easier and give excellent short term results. In a stable Child's A or B patient with minor ascites as well as suitable anatomy and hepatopedal flow, DSRS is the procedure of choice because it produces the smallest degree of HE postoperatively and increases the survival rate for nonalcoholics. If this is not feasible or if the surgeon lacks the technical expertise to perform DSRS, PCS is the logical alternative. In view of the data from the series observed in the United States, ablative procedures cannot be recommended at the present for the treatment of variceal bleeding. In the Child's C poor-risk patient, the operative mortality rate is prohibitive, and only nonsurgical means should be used to establish control of bleeding. In the elective situation, the surgical options change. The efficacy of ES as a definitive procedure to control recurrent variceal bleeding is unproved, and rebleeding can be significant; therefore, it cannot be recommended. H-grafts have a prohibitively high rate of long term thrombosis and are also not recommended, and the Linton or proximal splenorenal shunt offers no advantages over conventional portacaval shunting. Moreover, arterialization of the hepatic stumps of the portal vein does not prevent hepatic encephal

Topics: Acute Disease; Clinical Trials as Topic; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hepatic Encephalopathy; Humans; Hypertension, Portal; Liver Cirrhosis, Alcoholic; Portacaval Shunt, Surgical; Radiography; Recurrence; Sclerosing Solutions; Vasopressins

In recent years the technique of selective portasystemic shunting (Warren procedure) and sclerotherapy, and also the possibility of lowering portal pressure with beta-blockers, have changed the approach to management of patients with bleeding esophageal varices. Treatment of these patients is reviewed in the light of experience of 204 cases and the literature. The advantages and disadvantages of vasopressin, balloon tamponade, sclerotherapy, transhepatic embolization and various shunt and non-shunt operations in the acute phase are presented. For elective cases the discussion centers mainly on treatment by distal splenorenal shunt and sclerotherapy.

Topics: Acute Disease; Clinical Trials as Topic; Embolization, Therapeutic; Emergencies; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Lypressin; Portasystemic Shunt, Surgical; Prospective Studies; Recurrence; Sclerosing Solutions; Terlipressin; Vasopressins

Somatostatin (SST) has been shown by several controlled studies to be effective in halting acute severe bleeding from ulcerative and erosive lesions of the upper intestinal tract. Its efficacy for the treatment of bleeding esophageal varices is less certain, and more controlled studies are necessary. Intravenous administration of SST or subcutaneous application of the new synthetic SST-analogues produces a decrease in serum hormone levels and abolition of symptoms in patients with endocrine-active tumors such as vipoma, glucagonoma and carcinoid. SST has no effect on the outcome of acute pancreatitis, and experience with SST in treating intestinal fistulas is very limited.

Topics: Acute Disease; Cimetidine; Clinical Trials as Topic; Double-Blind Method; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Intestinal Fistula; Pancreatic Fistula; Pancreatitis; Paraneoplastic Endocrine Syndromes; Peptic Ulcer Hemorrhage; Prospective Studies; Random Allocation; Ranitidine; Secretin; Somatostatin; Vasopressins

Bleeding from esophageal varices is a feared complication of liver cirrhosis with high mortality. Pharmacotherapy of the acute bleeding episode with vasopressin has been shown to be effective in controlled studies, but side effects of this therapy are high and therefore replacement of vasopressin with somatostatin is under investigation. Another potential lead is the combination of vasopressin with vasodilators such as nitroglycerin. While acute pharmacotherapy of the patient with esophageal varices is well accepted, chronic or prophylactic pharmacotherapy is still in the investigative stage. Prophylactic therapy with beta-blockers, e.g. propranolol, has been shown to be effective in compensated patients with alcoholic cirrhosis. In patients with more advanced stages of the disease, or with cirrhosis of other etiology, the effectiveness of propranolol has not been proven. The mechanism of propranolol is similar to that of vasopressin, i.e. it lowers portal pressure by reducing portal flow. To maintain function of the affected organ, an alternative approach--namely lowering of portal pressure through reduction of the pathologically elevated resistance--should be actively investigated.

Topics: Acute Disease; Adrenergic beta-Antagonists; Chronic Disease; Clinical Trials as Topic; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Propranolol; Random Allocation; Somatostatin; Vasopressins

This study aims to explore the association between early administration of vasopressors and in-hospital mortality in acute pancreatitis (AP) patients admitted to the ICU.. The MIMIC-IV database was used to identify AP patients who had and had not received vasopressors. Univariate and multivariate logistic regression, propensity score matching (PSM), and inverse probability of treatment weighting (IPTW) were used for statistical analysis.. A total of 894 AP patients admitted to the ICU were included in the study. Among them, AP patients who received vasopressors were associated with an increased risk of in-hospital mortality in the unadjusted model (OR: 7.77, 95% CI 4.92-12.61, p<0.001), multivariable-adjusted model (OR: 2.51,95% CI 1.1-5.76, p<0.05), PSM model (OR: 2.58, 95% CI 1.03-6.85, p<0.05) and IPTW model (OR: 1.82, 95% CI 1.06-3.15, p<0.05) compared with patients who did not receive vasopressors. In the subgroup analysis, age (≥ 65 years old: OR: 2.5, 95% CI 0.82-7.91; <65 years old: OR: 4.63, 95% CI 0.84-26.41), male (OR: 1.19, 95% CI 0.35-4.03), ethnicity (white: OR: 2.49, 95% CI 0.81-7.62; non-white: OR: 4.28, 95% CI 0.85-23.7), usage of norepinephrine (OR: 2.29, 95% CI 0.91-5.78), and single-use of vasopressor (OR: 1.48, 95% CI 0.43-4.95) were not associated with in-hospital mortality in patients with AP, whereas vasopressin (OR: 4.27, 95% CI 1.24-15.13; p<0.05) and phenylephrine usage (OR: 4.75, 95% CI 1.66-13.95; p<0.05), combined vasopressor usage (OR: 4.41, 95% CI 1.55-12.96; p<0.01), and female usage (OR: 7.89, 95% CI 2.03-34.2; p<0.01) were associated with in-hospital mortality.. Early vasopressor use is significantly associated with increased in-hospital mortality among critically ill AP patients. This association might be greater in females, vasopressin, phenylephrine, and combined vasopressor users. Our results may benefit clinicians as they can guide the rational use of vasopressors in critically ill AP patients admitted to the ICU.

Topics: Acute Disease; Aged; Cohort Studies; Critical Illness; Female; Hospital Mortality; Humans; Intensive Care Units; Male; Pancreatitis; Phenylephrine; Retrospective Studies; Vasoconstrictor Agents; Vasopressins

BACKGROUND The aim of this study was to assess the impact of norepinephrine (NE), norepinephrine plus vasopressin (NE+VAS) and dopamine in patients with sepsis and heart failure. MATERIAL AND METHODS Data were extracted from the Medical Information Mart for Intensive Care III database, v1.4. Adults aged >18 years in an Intensive Care Unit (ICU) who had heart failure and took vasopressors were included. The patients were divided into 3 groups: NE, NE+VAS, and dopamine. Differences in survival, treatment time, and organ function among the 3 groups were compared. Propensity score matching (PSM) was used to screen for possible prognostic differences, and regression analysis was used to further analyze and predict prognoses. RESULTS A total of 1864 patients were included. There were significant differences among the 3 groups in 7-, 28-, and 90-day mortality after PSM. The 5-year survival rates among the 3 groups also were significantly different (P<0.001). After Cox regression analysis, NE+VAS was an independent risk factor affecting 5-year survival (P<0.001). After multiple linear regression, dopamine was the factor related to ICU and hospital lengths of stay. CONCLUSIONS Compared with NE or dopamine alone, NE+VAS can reduce survival in patients with sepsis and heart failure who need vasopressors. Compared with the other 2 treatment options, dopamine can shorten ICU and hospital stays for these patients.

Topics: Acute Disease; Aged; Cardiotonic Agents; Cohort Studies; Critical Illness; Dopamine; Female; Heart Failure; Humans; Length of Stay; Male; Norepinephrine; Retrospective Studies; Sepsis; Survival Rate; Vasoconstrictor Agents; Vasopressins

A novel treatment with intravenous levosimendan and vasopressin for new-onset acute pulmonary hypertension after weaning from cardiopulmonary bypass is described.. Retrospective analysis of a case series.. Single-center study.. Nineteen patients undergoing cardiac surgery exhibited new-onset acute pulmonary hypertension with acute right ventricular dysfunction after cardiopulmonary bypass.. Pulmonary hypertension with acute right heart dysfunction was treated with levosimendan as inodilator therapy and vasopressin combined with norepinephrine for systemic vasopressor therapy.. Mean pulmonary artery pressure decreased from 32 ± 9 to 26 ± 6 mmHg (p = 0.039) in the first 24 hours along with an increase in cardiac output (3.2 ± 1 to 4.2 ± 1.1 L/min; p = 0.012) and resolution of lactic acidosis. The ratio between mean pulmonary artery pressure and mean arterial pressure decreased from 1:2 to 1:3, and Wood units decreased from 3 ± 1 to 1.5 ± 2 (p = 0.042). At 30 days after intervention, 3 patients died.. The combination of levosimendan for inotropic support of the right ventricle in conjunction with its vasodilatory effect on the pulmonary circulation, along with the combination of vasopressin and norepinephrine for systemic vasopressor therapy, may be an effective alternative for the treatment of acute new-onset pulmonary hypertension and acute right heart dysfunction after cardiopulmonary bypass. Although there are many confounding variables in this case series, these findings justify additional sufficiently powered trials.

Topics: Acute Disease; Aged; Aged, 80 and over; Arterial Pressure; Cardiopulmonary Bypass; Cardiotonic Agents; Dose-Response Relationship, Drug; Drug Therapy, Combination; Female; Follow-Up Studies; Humans; Hypertension, Pulmonary; Injections, Intravenous; Male; Retrospective Studies; Simendan; Treatment Outcome; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

A 57-year-old woman with pre-dialysis chronic kidney disease (CKD) was hospitalized because of fever and fatigue. On admission, increased inflammatory response and pyuria with bacteriuria were observed. Pyelonephritis was successfully treated with antibiotics, whereas her fatigue continued and she developed progressive hypercalcemia and hyponatremia; serum sodium level, 116 mEq/L and corrected serum calcium level, 13.4 mg/dL. Plasma concentrations of adrenocorticotropic hormone and cortisol and serum luteinizing hormone were under the detection level. Although the reaction of other anterior pituitary hormones and the serum antidiuretic hormone (ADH) was preserved, the response of serum luteinizing hormone to administration of luteinizing hormone releasing hormone was impaired. Magnetic resonance imaging showed no structural abnormality in the thalamus, hypothalamus, and pituitary gland. She was diagnosed with adrenal insufficiency caused by partial hypopituitarism in concomitant with pyelonephritis. After starting hydrocortisone replacement, serum levels of sodium and calcium were rapidly normalized. This case highlights the importance of adrenal insufficiency as a differential diagnosis of hypercalcemia in patients with pre-dialysis CKD, especially when hyponatremia was concomitantly observed. Besides, infection should be considered as an important trigger for the development of latent adrenal insufficiency since it could increase the physiological demand of corticosteroid in the body. Also, CKD may enhance the magnitude of hypercalcemia since CKD patients have decreased capacity to increase urinary calcium excretion.

Topics: Acute Disease; Adrenal Insufficiency; Adrenocorticotropic Hormone; Diagnosis, Differential; Dialysis; Female; Humans; Hydrocortisone; Hypercalcemia; Hyponatremia; Hypopituitarism; Luteinizing Hormone; Magnetic Resonance Imaging; Middle Aged; Pyelonephritis; Renal Insufficiency, Chronic; Treatment Outcome; Vasopressins

A pulmonary hypertensive crisis (PHC) can be a life-threatening condition. We established a PHC model by exposing rats with monocrotaline (MCT)-induced pulmonary hypertension to acute hypoxia, and investigated the effects of vasopressin, phenylephrine, and norepinephrine on the PHC.. Four weeks after MCT 60 mg kg. PHC was associated with increased RV dilatation and paradoxical septal motion. Vasopressin increased MBP [mean (standard error)] from 52.6 (3.8) to 125.0 (8.9) mm Hg and CI from 25.4 (2.3) to 40.6 (1.8) ml min. In this rat model of a PHC, vasopressin, but not phenylephrine or norepinephrine, resulted in better haemodynamic and vascular recovery.

Topics: Acute Disease; Animals; Drug Evaluation, Preclinical; Echocardiography; Hemodynamics; Hypertension, Pulmonary; Hypoxia; Male; Monocrotaline; Nordefrin; Oxygen; Partial Pressure; Phenylephrine; Rats, Sprague-Dawley; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

Hyponatremia is a common feature of acute illness and associated with increased mortality. This may be explained by a stress-mediated activation of the vasopressin system with an increase in free-water reabsorption.. To investigate whether the association between hyponatremia and mortality could be explained by activation of the vasopressin system.. We prospectively enrolled adult, medical patients seeking emergency care in three centres in Switzerland, France and the United States. We investigated associations between admission plasma sodium and copeptin, a stable portion of the vasopressin-precursor peptide, with 30-day mortality. We performed uni- and multivariate regression analysis.. Of 6962 included patients, 18% had hyponatremia (sodium ≤135 mmol L. This prospective study including medical patients upon emergency room admission found hyponatremia as well as an activation of the vasopressin system to be independently associated with mortality. This suggests that stress- and vasopressin-independent mechanisms are responsible for the association of low sodium levels with mortality.

Topics: Acute Disease; Adult; Aged; Cohort Studies; Correlation of Data; Cross-Cultural Comparison; Emergency Service, Hospital; Female; France; Glycopeptides; Humans; Hyponatremia; Male; Middle Aged; Prospective Studies; Risk; Secretory Rate; Sodium; Switzerland; United States; Vasopressins

Empathy defined as the ability to understand and the share the feelings, thoughts, and attitudes of another, is an important skill in survival and reproduction. Among many factors that affect empathy include psychological stress, anxiety states. The aim of this study was to investigate the impact of acute psychological stress on empathic behavior and its association with oxytocin and vasopressin levels in amygdala and prefrontal cortex. Rats were subjected to 0.2 mA (low) and 1.6 mA (high) intensity of foot shock stress for duration of 20 min. Empathic behavior was found to be improved as a response to low intensity stress, but not to high intensity stress. As a response to lower intensity stress, vasopressin was increased in prefrontal cortex and amygdala; oxytocin was increased in only prefrontal cortex, and corticosterone levels increased in general. Anxiety indicators did not change in low intensity stress group yet; high intensity stress group demonstrated a lesser degree of anxiety response. High intensity stress group stayed unexpectedly more active in middle area of elevated plus maze test equipment, which may support impaired executive decision making abilities in the setting of high anxiety states. Further research is needed to investigate gender effects, the role of dopaminergic system and other stress related pathways in acute stress.

Topics: Acute Disease; Animals; Anxiety; Brain; Electroshock; Empathy; Male; Motor Activity; Oxytocin; Rats, Sprague-Dawley; Social Behavior; Stress, Psychological; Vasopressins

We conducted this study to assess the clinical application of obestatin and arginine vasopressin (AVP) levels in cases of acute renal failure (ARF) and acute heart failure (AHF).. 30 cases of ARF, 30 cases of AHF, 30 cases of ARF complicated with AHF, and 30 cases of healthy subjects (control group) were successively selected. An ELISA test was conducted to detect levels of obestatin and AVP. Routine biochemistry testing was applied to detect the levels of serum creatinine and calculate the glomerular filtration rate (GFR). Electrochemiluminescence double antibody sandwich fluorescence immune testing was applied to detect NT-proBNP and color Doppler ultrasound diagnostic apparatus was applied to detect renal arterial resistive index (RI) and left ventricular ejection fraction (LVEF). The 30-day mortality was documented.. Compared to other groups, the group of patients suffering from ARF complicated with AHF had significantly higher levels of obestatin and AVP, and significantly higher levels of serum creatinine, NT-proBNP and RI; however, their GFR and LVEF levels were the lowest. Differences were statistically significant (p < 0.05). Levels of obestatin and AVP are positively correlated with serum creatinine, NT-proBNP and RI levels, but negatively correlated with GFR and LVEF levels. The mortality rate of the group suffering from ARF complicated with AHF was markedly increased (p = 0.035). The obestatin and AVP levels of the death group were significantly higher than that of the survival group. However, the comparison among levels of serum creatinine, GFR, NT-proBNP, RI and LVEF revealed no statistical significance (p > 0.05).. Obestatin and AVP levels were closely related to the severity of ARF and AHF and survival prognosis, which could be a sensitive indicator for diagnoses and prognoses.

Topics: Acute Disease; Acute Kidney Injury; Adult; Aged; Female; Ghrelin; Glomerular Filtration Rate; Heart Failure; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Neurophysins; Peptide Fragments; Protein Precursors; Vasopressins; Ventricular Function, Left

In this article, we present a clinical case of refractory septic shock resulting from intestinal perforation treated with high doses of vasopressin and hydrocortisone during emergency surgery. The use of such high doses of vasopressin for this type of shock is not described in the literature.. A 49-year-old white woman with grade III obesity, Crohn's disease, and an intestinal perforation presented with refractory septic shock. Initially, a low dose of vasopressin was used. Then, the dosage was increased to 0.4 U/minute; in the literature, this is defined as "salvage therapy." This therapy consists of an initial load followed by a continuous infusion of hydrocortisone.. The significant increase in her cardiac index and stroke volume index resulted in an improvement in peripheral resistance, gas exchange, and urine output and a decrease in her heart rate, interleukin-6 level, and tumor necrosis factor-α level. The administration of high doses of vasopressin and corticosteroids was demonstrated to be safe for the immune system, to reduce the systemic inflammatory response, and to have direct cardiovascular effects. Further studies are required to examine the use of vasopressin as an initial vasopressor as well as its use in high dosages and in combination with corticosteroids.

Topics: Acute Disease; Anti-Inflammatory Agents; Crohn Disease; Drug Therapy, Combination; Female; Humans; Hydrocortisone; Ileocecal Valve; Intestinal Perforation; Middle Aged; Obesity, Morbid; Shock, Septic; Tomography, X-Ray Computed; Vasoconstrictor Agents; Vasopressins

Topics: Acidosis, Lactic; Acute Disease; Administration, Intravenous; Adult; Aged; Alcoholism; Anti-Bacterial Agents; Bicarbonates; Comorbidity; Confusion; Glasgow Coma Scale; Humans; Hyperlactatemia; Hypotension; Intubation, Intratracheal; Male; Norepinephrine; Respiration, Artificial; Respiratory Insufficiency; Tachycardia; Thiamine; Vasoconstrictor Agents; Vasopressins; Vitamin B Complex

Hypopituitarism after hypovolemic shock is well established in certain patient cohorts. However; the effects of hemorrhagic shock on pituitary function in trauma patients remains unknown. The aim of this study was to assess pituitary hormone variations in trauma patients with hemorrhagic shock.. Patients with acute traumatic hemorrhagic shock presenting to our level 1 trauma center were prospectively enrolled. Hemorrhagic shock was defined as systolic blood pressure (SBP) ≤ 90 mmHg on arrival or within 10 minutes of arrival in the emergency department, and requirement of ≥2 units of packed red blood cell transfusion. Serum cortisol and serum pituitary hormones (vasopressin [ADH], adrenocorticotrophic hormone [ACTH], thyroid stimulating hormone [TSH], follicular stimulating hormone [FSH], and luteinizing hormone [LH]) were measured in each patient on admission and at 24, 48, 72, and 96 hours after admission. Outcome measure was variation in pituitary hormones.. A total of 42 patients were prospectively enrolled; mean age was 37 ± 12 years, mean SBP 85.4 ± 64.5 mmHg, and median Injury Severity Score was 26 (range 18 to 38). There was an increase in the levels of cortisol (p < 0.001), a decrease in the levels of ACTH (p < 0.001) and ADH (p < 0.001), but no change in the levels of LH (p = 0.30), FSH (p = 0.07), and TSH (p = 0.89) over 96 hours. Ten patients died during their hospital stay. Patients who died had higher mean admission ADH levels (p = 0.03), higher mean admission ACTH levels (p < 0.001), and lower mean admission cortisol levels (p = 0.04) compared with patients who survived.. Acute hypopituitarism does not occur in trauma patients with acute hemorrhagic shock. In patients who died, there was a decrease in cortisol levels, which appears to be adrenal in origin.

Topics: Acute Disease; Adrenocorticotropic Hormone; Adult; Aged; Biomarkers; Female; Humans; Hydrocortisone; Hypopituitarism; Luteinizing Hormone; Male; Middle Aged; Prospective Studies; Shock, Hemorrhagic; Thyrotropin; Vasopressins; Wounds and Injuries

To report a novel technique and preliminary clinical outcomes in managing lower gastrointestinal bleeding (LGIB).. Eighteen LGIB patients (11 men and 7 women, mean age: 66.2 years) were treated with artificially induced vasospasm therapy by semi-selective catheterization technique. Epinephrine bolus injection was used to initiate the vascular spasm, and followed by a small dose vasopressin infusion (3-5 units/h) for 3h. The technical success, clinical success, recurrent bleeding and major complications of this study were evaluated and reported.. Sixteen bleeders were in the superior mesenteric artery and 2 in the inferior mesenteric artery. All patients achieved successful immediate hemostasis. Early recurrent bleeding (<30 days) was found in 4 patients with local and new-foci re-bleeding in 2 (11.1%) each. Repeated vasospasm therapy was given to 3 patients, with clinical success in 2. Technical success for the 21 bleeding episodes was 100%. Lesion-based and patient-based primary and overall clinical successes were achieved in 89.4% (17/19) and 77.7% (14/18), and 94.7% (18/19) and 88.8% (16/18), respectively. None of our patients had complications of bowel ischemia or other major procedure-related complications. The one year survival of our patients was 72.2 ± 10.6%.. Pharmaco-induced vasospasm therapy seems to be a safe and effective method to treat LGIB from our small patient-cohort study. Further evaluation with large series study is warranted. Considering the advanced age and complex medical problems of these patients, this treatment may be considered as an alternative approach for interventional radiologists in management of LGIB.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Angiography; Catheterization; Contrast Media; Endpoint Determination; Epinephrine; Female; Gastrointestinal Hemorrhage; Hemostatic Techniques; Humans; Male; Middle Aged; Survival Rate; Treatment Outcome; Vasoconstriction; Vasopressins

In women with chronic schizophrenia, higher levels of peripheral oxytocin have been associated with lower levels of positive but not negative symptoms. Sex-specific associations between endogenous levels of oxytocin (OT) and arginine vasopressin (AVP) with clinical symptoms and cognition in untreated early course patients have not been examined.. Clinical ratings and neuropsychological testing were performed in thirty-eight acutely ill, unmedicated first-episode schizophrenia patients (14 women, 24 men). Serum hormone assays were obtained in patients and thirty-eight demographically similar healthy controls.. Patients demonstrated increased AVP levels compared to controls (p = 0.01). Higher AVP levels were associated with greater positive symptoms (r = 0.58, p = 0.03) and worse verbal learning (r = -0.63, p = 0.02) in female, but not male, patients. OT levels did not statistically differ between patients and controls, and were unrelated to clinical symptoms or cognition in patients.. Results suggest an association of endogenous AVP with increased positive symptom severity and worse cognition in untreated female, but not male, schizophrenia patients. Findings support the role of neuroendocrine alterations in acute psychosis and the importance of examining sex-specific neuroendocrine alterations early in the course of schizophrenia.

Topics: Acute Disease; Adolescent; Adult; Analysis of Variance; Female; Humans; Learning Disabilities; Linear Models; Male; Neuropsychological Tests; Oxytocin; Psychiatric Status Rating Scales; Psychotic Disorders; Sex Characteristics; Vasopressins; Verbal Learning; Young Adult

Hospitalizations for acute heart failure syndromes (AHFS) are associated with high post-discharge morbidity and mortality. The potential role of vasopressin antagonists (VA) in AHFS was presented at the 2008 European Society of Cardiology Working Group on Acute Cardiac Care Meeting held in Versailles, France from 25-28 October 2008. This report represents a summary of the presentation at this meeting.

Topics: Acute Disease; Congresses as Topic; France; Heart Failure; Hormone Antagonists; Humans; Treatment Outcome; Vasopressins; Ventricular Remodeling

Topics: Acute Disease; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Diuresis; Heart Failure; Humans; Receptors, Vasopressin; Vasopressins

Limbic and cortical neurocircuits profoundly influence hypothalamic-pituitary-adrenal (HPA) axis responses to stress yet have little or no direct projections to the hypothalamic paraventricular nucleus (PVN). Numerous lines of evidence suggest that the bed nucleus of the stria terminalis (BST) is well positioned to relay limbic information to the PVN. The BST comprises multiple anatomically distinct nuclei, of which some are known to receive direct limbic and/or cortical input and to heavily innervate the PVN. Our studies test the hypothesis that subregions of the BST differentially regulate HPA axis responses to acute stress. Male Sprague Dawley rats received bilateral ibotenate lesions, targeting either the principal nucleus in the posterior BST or the dorsomedial/fusiform nuclei in the anteroventral BST. Posterior BST lesions elevated plasma ACTH and corticosterone in response to acute restraint stress, increased stress-induced PVN c-fos mRNA, and elevated PVN corticotropin-releasing hormone (CRH) and parvocellular arginine vasopressin (AVP) mRNA expression relative to sham-lesion animals. In contrast, anterior BST lesions attenuated the plasma corticosterone response and decreased c-fos mRNA induction in the PVN but did not affect CRH and parvocellular AVP mRNA expression in the PVN. These data suggest that posterior BST nuclei are involved in inhibition of the HPA axis, whereas the anteroventral BST nuclei are involved in HPA axis excitation. The results indicate that the BST contains functional subdomains that play different roles in integrating and processing limbic information in response to stress and further suggest that excitatory as well as inhibitory limbic information is funneled through these important cell groups.

Topics: Acute Disease; Adrenal Glands; Adrenocorticotropic Hormone; Animals; Body Weight; Corticosterone; Corticotropin-Releasing Hormone; Glutamate Decarboxylase; Hypothalamo-Hypophyseal System; Isoenzymes; Limbic System; Male; Organ Size; Paraventricular Hypothalamic Nucleus; Pituitary-Adrenal System; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; Restraint, Physical; RNA, Messenger; Septal Nuclei; Stress, Physiological; Thymus Gland; Vasopressins

To assess the prevalence of hypopituitarism following traumatic brain injury (TBI), describe the time-course and assess the association with trauma-related parameters and early post-traumatic hormone alterations.. A 12-month prospective study.. Forty-six consecutive patients with TBI (mild: N = 22; moderate: N = 9; severe: N = 15).. Baseline and stimulated hormone concentrations were assessed in the early phase (0-12 days post-traumatically), and at 3, 6 and 12 months postinjury. Pituitary tests included the Synacthen-test (acute +6 months) and the insulin tolerance test (ITT) or the GHRH + arginine test if the ITT was contraindicated (3 + 12 months). Insufficiencies were confirmed by retesting.. Early post-traumatic hormone alterations mimicking central hypogonadism or hypothyroidism were present in 35 of the 46 (76%) patients. Three months post-traumatically, 6 of the 46 patients failed anterior pituitary testing. At 12 months, one patient had recovered, whereas none developed new insufficiencies. All insufficient patients had GH deficiency (5 out of 46), followed by ACTH- (3 out of 46), TSH- (1 out of 46), LH/FSH- (1 out of 46) and ADH deficiency (1 out of 46). Hypopituitary patients had more frequently been exposed to severe TBI (4 out of 15) than to mild or moderate TBI (1 out of 31) (P = 0.02). Early endocrine alterations including lowered thyroid and gonadal hormones, and increased total cortisol, free cortisol and copeptin were positively associated to TBI severity (P < 0.05), but not to long-term development of hypopituitarism (P > 0.1), although it was indicative in some.. Long-term hypopituitarism was frequent only in severe TBI. During the 3-12 months follow-up, recovery but no new insufficiencies were recorded, indicating manifest hypothalamic or pituitary damage already a few months postinjury. Very early hormone alterations were not associated to long-term post-traumatic hypopituitarism. Clinicians should, nonetheless, be aware of potential ACTH deficiency in the early post-traumatic period.

Topics: Acute Disease; Adolescent; Adrenocorticotropic Hormone; Adult; Brain Injuries; Case-Control Studies; Female; Gonadotropins, Pituitary; Growth Hormone; Humans; Hypopituitarism; Logistic Models; Male; Middle Aged; Odds Ratio; Pituitary Function Tests; Prospective Studies; Thyrotropin; Time; Vasopressins

Disorders of water and sodium balance are frequently seen in patients with severe brain injury (SBI), and may worsen their prognosis.. To evaluate vasopressin (AVP) serum levels and sodium and water balance disorders during the first week post-injury in patients with SBI.. Thirty-six adult patients with SBI (admission Glasgow Coma Scale score < or= 8) and an estimated time of injury

Topics: Acute Disease; Adult; Biomarkers; Brain Injuries; Case-Control Studies; Female; Glasgow Coma Scale; Humans; Male; Osmolar Concentration; Prospective Studies; Sodium; Vasopressins; Water-Electrolyte Imbalance

Coronary effects of endothelin-1 and vasopressin during acute hypotension, and the role of NO and prostanoids in these effects were examined in anesthetized goats. Left circumflex coronary artery flow was measured electromagnetically, and hypotension was induced by constriction of the caudal vena cava in animals non-treated (7 goats) or treated with the inhibitor of NO synthesis N(w)-nitro-L-arginine methyl esther (L-NAME, 5 goats), the cyclooxygenase inhibitor meclofenamate (5 goats) or both drugs (5 goats). Under normotension (22 goats), mean arterial pressure averaged 93 +/- 3 mm Hg and coronary vascular conductance (CVC) 0.37 +/- 0.025 ml/min/mm Hg. Endothelin-1 (0.01-0.3 nmol) and vasopressin (0.03-1 nmol), intracoronarily injected, dose-dependently decreased CVC by up to 56% for endothelin-1 and 40% for vasopressin. During hypotension in every condition tested, mean arterial pressure decreased to approximately 60 mm Hg, and CVC only decreased during hypotension pretreated with L-NAME (23%) or L-NAME + meclofenamate (34%). Under non-treated hypotension, the decreases in CVC by endothelin-1 were augmented approximately 1.5 fold, and those by vasopressin were not modified. This increase in CVR by endothelin-1 was not affected by L-NAME and was reversed by meclofenamate or L-NAME + meclofenamate. The coronary effects of vasopressin were not modified by any of these treatments. Therefore, acute hypotension increases the coronary vasoconstriction in response to endothelin-1 but not to vasopressin. This increased response to endothelin-1 may be related to both inhibition of NO release and release of vasoconstrictor prostanoids.

Topics: Acute Disease; Anesthesia; Animals; Blood Pressure; Coronary Circulation; Cyclooxygenase Inhibitors; Disease Models, Animal; Endothelin-1; Female; Goats; Hypotension; Meclofenamic Acid; NG-Nitroarginine Methyl Ester; Nitric Oxide; Vasoconstriction; Vasopressins

An elevation of the plasma antidiuretic hormone (ADH) levels has frequently been observed in Meniere's disease patients. However, little is known regarding the mechanism behind such an elevation of ADH level in Meniere's disease patients. Therefore, we measured the plasma ADH in Meniere's disease patients and other vertigo patients to elucidate the association between the ADH levels, stress levels and the development of Meniere's symptom.. The plasma ADH levels and plasma osmotic pressure were determined in 23 definite Meniere's disease patients and 160 patients with other types of vertigo/dizziness. All participants were administered questionnaire regarding their psychological status including their stress levels.. The ADH levels of Meniere's disease patients in the acute phase (5.80 +/- 1.37 pg/mL) were significantly higher in comparison with that of Meniere's disease patients in the remission phase (2.26 +/- 0.41 pg/mL) (P < 0.05). In other peripheral vertigo patients, the ADH level in the acute phase (1.71 +/- 0.23 pg/mL) was not significantly different from that in the remission phase (1.45 +/- 0.15 pg/mL). Meniere's disease patients in the acute phase had a significantly higher stress score (114 +/- 23) than Meniere's disease patients in the remission phase (56 +/- 13) (P < 0.05). However, there was no significant correlation between their stress score and the ADH levels.. These results suggest that the elevation of the plasma ADH levels in Meniere's disease patients in the acute phase is, therefore, associated with the pathogenesis of Meniere's disease attacks rather than with stress.

Topics: Acute Disease; Adult; Aged, 80 and over; Depression; Dizziness; Female; Humans; Life Change Events; Male; Meniere Disease; Middle Aged; Osmotic Pressure; Remission, Spontaneous; Sex Factors; Stress, Psychological; Vasopressins; Vertigo

Although acute decreases in plasma volume are known to enhance the osmotically induced arginine vasopressin (AVP) release, it is unclear whether there is also such interaction at the level of gene transcription. It also remains to be established how sustained changes in plasma volume affect the osmoregulation. In this study, we examined how acute and chronic decreases in blood volume affected the osmoregulation of AVP release and gene transcription in rats. Acute hypovolemia was induced by intraperitoneal injection of polyethylene glycol (PEG), and chronic hypovolemia was induced by 3 days of water deprivation (WD) or 12 days of salt loading (SL). Rats were injected with isotonic or hypertonic saline, and plasma AVP levels and AVP heteronuclear (hn)RNA expression in the supraoptic and paraventricular nuclei, an indicator of gene transcription, were examined in relation to plasma osmolality in each group. Plasma AVP levels were correlated with plasma Na levels in all groups. Whereas the regression lines relating plasma AVP to Na were almost identical among control, WD, and SL groups, the thresholds of plasma Na for AVP release were significantly decreased only in the PEG group. AVP hnRNA levels were also correlated with plasma Na levels in control and PEG groups, and the thresholds were significantly decreased in the PEG group. In contrast, there was no significant correlation of AVP hnRNA and plasma Na levels in WD and SL groups. Thus it was demonstrated that acute and chronic reduction in plasma volume affected the osmoregulation of AVP release and gene transcription in different ways.

Topics: Acute Disease; Animals; Blood Proteins; Chronic Disease; Gene Expression Regulation; Hypovolemia; Male; Plasma Volume; Polyethylene Glycols; Rats; Rats, Sprague-Dawley; Sodium; Transcription, Genetic; Vasopressins; Water-Electrolyte Balance

Endotoxemia can lead to fluid metabolism alterations despite unchanged or elevated plasma vasopressin (VP) levels, suggesting a refractoriness of the kidney to the effect of the peptide. To test this hypothesis, we examined the effect of lipopolysaccharide (LPS) injection on the expression of V2 receptors and aquaporin-2 in the kidney.. Plasma VP and urine osmolality, and binding of [3H]VP to kidney membranes, Western blot, and immunohistochemical analysis of aquaporin-2, in situ hybridization for V2 VP receptors and cytokines mRNAs were measured in the kidney 3 to 24 hours after LPS injection, 250 microg/100 g, intraperitoneally.. LPS injection caused prolonged decreases in urine osmolality (up to 24 hours) without significant changes in plasma levels of sodium or VP. This was associated with marked decreases in V2 VP receptor mRNA and VP receptor number in the kidney, which were evident for up to 12 hours after LPS injection. Aquaporin-2 in kidney inner medulla was also reduced by about 50%. LPS induced interleukin (IL)-1beta in the kidney medulla by 3 hours, reached maximum at 6 hours, and started to decline by 12 hours, while it increased IL-6 mRNA significantly only at 3 hours. Interleukin mRNA expression was absent in kidneys of control rats. In vitro incubation of kidney medulla slices with IL-1beta reduced VP binding.. The inflammatory response to acute endotoxemia down regulates V2 VP receptors and aquaporin-2 of the kidney inner medulla resulting in prolonged impairment of the renal capacity to concentrate urine.

Topics: Acute Disease; Animals; Aquaporin 2; Aquaporins; Down-Regulation; Endotoxemia; Interleukin-1; Interleukin-6; Kidney Concentrating Ability; Kidney Medulla; Lipopolysaccharides; Male; Osmolar Concentration; Rats; Rats, Wistar; Receptors, Vasopressin; RNA, Messenger; Sodium; Tritium; Urine; Vasopressins

The use of vasopressin for the treatment of septic shock is increasing. Few reports of fluid and electrolyte complications of this therapy have been reported. A neurologically impaired, 53-year-old man with a history of syndrome of inappropriate antidiuretic hormone developed apparent transient diabetes insipidus and acute hypernatremia after being treated with vasopressin. He was treated for presumed septic shock with intravenous vasopressin 0.01-0.10 U/minute. His blood pressure did not improve with this therapy, and his course was complicated by hyponatremia during the vasopressin infusion. Discontinuation of the infusion was followed by a profound (8.4 L) diuresis and rapid onset of hypernatremia (serum sodium concentration increased from 132 to 157 mEq/L over 8 hrs). Although urine osmolality was not measured during the patient's diuresis, the rapid changes in serum sodium concentration can be explained only by an inappropriate water diuresis. The diuresis ceased when the vasopressin infusion was resumed. We concluded that these findings are most consistent with transient diabetes insipidus. The safety and efficacy of intravenous vasopressin have not been established in patients with septic shock and underlying disorders of water homeostasis. The drug may have diminished vasoconstrictive effects in this patient population. Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock.

Topics: Acute Disease; Diabetes Insipidus; Humans; Hypernatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasoconstrictor Agents; Vasopressins

Topics: Acute Disease; Child; Energy Metabolism; Fluid Therapy; Humans; Hyponatremia; Isotonic Solutions; Sodium Chloride; Urination; Vasopressins; Water-Electrolyte Balance

This study investigated the effects of fetal treatment with dexamethasone on ovine fetal cardiovascular defence responses to acute hypoxaemia, occurring either during or 48 h following the period of glucocorticoid exposure. To address the mechanisms underlying these responses, chemoreflex function and plasma concentrations of catecholamines, neuropeptide Y (NPY) and vasopressin were measured. Under general halothane anaesthesia, 26 Welsh Mountain sheep fetuses were surgically prepared for long-term recording at between 117 and 120 days of gestation (dGA; term is approximately 145 days) with vascular catheters and a Transonic flow probe around a femoral artery. Following at least 5 days of recovery, fetuses were randomly assigned to one of two experimental groups. After 48 h of baseline recording, at 125 +/- 1 dGA, half of the fetuses (n = 13) were continuously infused I.V. with dexamethasone for 48 h at a rate of 2.06 +/- 0.13 microg kg-1 h-1. The remaining 13 fetuses were infused with heparinized saline at the same rate (controls). At 127 +/- 1 dGA, 2 days from the onset of infusions, seven fetuses from each group were subjected to 1 h of acute hypoxaemia. At 129 +/- 1 dGA, 2 days after the end of infusions, six fetuses from each group were subjected to 1 h of acute hypoxaemia. Similar reductions in fetal partial pressure of arterial oxygen occurred in control and dexamethasone-treated fetuses during the acute hypoxaemia protocols. In control fetuses, acute hypoxaemia led to transient bradycardia, femoral vasoconstriction and significant increases in plasma concentrations of catecholamines, vasopressin and NPY. In fetuses subjected to acute hypoxaemia during dexamethasone treatment, the increase in plasma NPY was enhanced, the bradycardic response was prolonged, and the plasma catecholamine and vasopressin responses were diminished. In fetuses subjected to acute hypoxaemia 48 h following dexamethasone treatment, femoral vasoconstriction and plasma catecholamine and vasopressin responses were enhanced, whilst the prolonged bradycardia and augmented plasma NPY responses persisted. These data show that fetal treatment with dexamethasone modifies the pattern and magnitude of fetal cardiovascular responses to acute oxygen deprivation. Modifications to different mechanisms mediating the fetal defence responses to acute hypoxaemia that occur during dexamethasone treatment may reverse, persist or even become enhanced by 48 h following the treatment period.

Topics: Acid-Base Equilibrium; Acute Disease; Animals; Blood Pressure; Carbon Dioxide; Catecholamines; Chemoreceptor Cells; Dexamethasone; Endocrine System; Female; Fetus; Glucocorticoids; Heart Rate, Fetal; Hypoxia; Neuropeptide Y; Oxygen; Pregnancy; Regional Blood Flow; Sheep; Vascular Resistance; Vasopressins

To investigate the changes and clinical significance of arginine vasopressin (AVP) in elderly patients with acute traumatic cerebral injury.. With radioimmunoassay, the plasma levels of AVP were measured in 32 elderly patients with acute traumatic cerebral injury, 30 traumatic patients without cerebral injury and 30 healthy elderly volunteers, respectively.. The plasma level of AVP in patients with acute traumatic cerebral injury in the early stage (48.30 ng/L +/- 8.28 ng/L) was much higher than that of the traumatic patients without cerebral injury (25.56 ng/L +/- 4.64 ng/L, P<0.01), which was much higher than that of the healthy volunteers (5.06 ng/L +/- 4.12 ng/L, P<0.01). The level of AVP in the patients with acute traumatic cerebral injury was negatively related with GCS scores.. AVP may play an important role in the pathophysiological process in patients with acute traumatic cerebral injury in the early stage. The severer the cerebral injury is, the higher the level of AVP is, which indicates that the level of AVP may be one of the severity indices of traumatic cerebral injury in elderly patients.

Topics: Acute Disease; Aged; Aged, 80 and over; Brain Injuries; Female; Glasgow Coma Scale; Humans; Injury Severity Score; Male; Middle Aged; Neurophysins; Protein Precursors; Vasopressins

The role of vasopressin, cosecreted with corticotropin-releasing hormone (CRH), in stress is debated, because both normal as well as reduced adrenocorticotropin hormone (ACTH) rise to an acute challenge has been reported in Brattleboro rats genetically lacking vasopressin (di/di). Because di/di pups could be born either from di/+ (heterozygous) or from di/di mothers, and maternal influence is known to modify adult responsiveness, we investigated whether the influence of maternal genotype could explain the variability. Adult rats from mothers with different genotypes were stressed with 60 min restraint and trunk blood was collected for measuring hormone content by radioimmunoassay at the end of stress. All offspring of di/+ mothers had similar ACTH responses to restraint, while the di/di rats born to, and raised by di/di mothers showed reduced ACTH reactivity to restraint. The di/di rats showed elevated water turnover and required a daily cage cleaning every day, which meant frequent handling. To offset the role of handling, all rats had daily cage cleaning in the next series, but the results were the same as in the first series. To investigate whether lactation, the behaviour of the mother or some other factor during the pregnancy is responsible for the differences, pups from di/+ dams were raised by di/di foster mothers and vice versa. We found that the genotype of parental mother is more important than that of the foster mother. The corticosterone and prolactin elevation normally seen after acute stress was unchanged by family history, maternal or personal genotype. Furthermore, in studies with mutant animals, the rearing conditions should be controlled by the experimenter. In experiments with Brattleboro rats, the use of homozygous and heterozygous rats from the same litters of di/+ dams and di/di males is recommended. Our results suggest that vasopressin is not indispensable for ACTH release, and that the di/di genotype of the parental mother can decrease the stress reactivity of the di/di Brattleboro rats.

Topics: Acute Disease; Adrenocorticotropic Hormone; Animals; Corticosterone; Female; Genotype; Heterozygote; Homozygote; Male; Pregnancy; Prolactin; Rats; Rats, Brattleboro; Restraint, Physical; Stress, Physiological; Vasopressins

This study compares the haemodynamic and hormonal responses during haemorrhage of conscious dogs pre-treated with an endothelin-A (ET-A) receptor inhibitor. The dogs were studied in two different randomized groups: the control group and a group that was given the ET-A receptor antagonist ABT-627 (as a bolus of 1 mg x kg of body weight(-1) followed by 0.01 mg x kg body weight(-1) x min(-1) intravenously). The time-course was the same for both groups: after a 1 h baseline period (pre-haemorrhage), blood (25 ml x kg of body weight(-1)) was withdrawn within 5 min. Haemodynamics were continuously recorded and hormone levels measured after 1 h (post-haemorrhage). Thereafter, the blood withdrawn was retransfused within 5 min and haemodynamics again observed for 1 h (post-retransfusion). In ABT-627-treated dogs, the decrease in mean arterial pressure from 87+/-3 to 64+/-3 mmHg (P<0.05 versus pre-haemorrhage), and cardiac output from 2.1+/-0.1 to 1.3+/-0.1 l x min(-1) (P<0.05 versus pre-haemorrhage) and the increase in systemic vascular resistance from 3286+/-174 to 4211+/-230 dyn.s.cm(-5) (P<0.05 versus pre-haemorrhage) during acute haemorrhage are comparable with controls. During haemorrhage in controls, vasopressin levels increased from 0+/-0 to 13+/-2 pg x ml(-1) (P<0.05 versus pre-haemorrhage), angiotensin II levels increased from 9+/-1 to 28+/-9 pg x ml(-1) (P<0.05 versus pre-haemorrhage) and adrenaline levels increased from 134+/-22 to 426+/-74 pg x ml(-1) (P<0.05 versus pre-haemorrhage) whereas noradrenaline levels did not change (approx. 200 pg x ml(-1)). In ABT-627-treated dogs, vasopressin levels increased from 0.2+/-0.0 to 22.2+/-6.1 pg x ml(-1) (P<0.05 versus pre-haemorrhage and P<0.05 versus control), angiotensin II levels increased from 8+/-1 to 37+/-8 pg x ml(-1) (P<0.05 versus pre-haemorrhage), noradrenaline levels increased from 147+/-16 to 405+/-116 pg x ml(-1) (P<0.05 versus pre-haemorrhage) and adrenaline levels did not change (200 pg x ml(-1)) during haemorrhage. We conclude from our results that dogs receiving the selective ET-A inhibitor ABT-627 seem to show a different hormonal response after haemorrhage compared with controls, displaying considerably higher noradrenaline concentrations. Independent of ET-A receptor inhibition, cardiac output during haemorrhage was maintained within the control range. This may indicate that the organism is defending blood flow (cardiac output) over blood pressure during haemorrhage, and that this defence s

Topics: Action Potentials; Acute Disease; Angiotensin II; Animals; Atrasentan; Blood Pressure; Cardiac Output; Dogs; Endothelin Receptor Antagonists; Endothelin-1; Hemorrhage; Norepinephrine; Pyrrolidines; Random Allocation; Receptor, Endothelin A; Vascular Resistance; Vasodilator Agents; Vasopressins

To determine the impact of hypertonic saline administration upon rat arginine vasopressin (AVP) gene transcription in supraoptic nucleus neurons, a probe complementary to the first intron (AVP1) of AVP was used to measure changes in AVP heteronuclear RNA (hnRNA) levels. Animals that received hypertonic saline had increases in AVP1 after 15 and 30 min, with a return to baseline levels by 180 min. In a double injection paradigm, animals were given an injection of normal or hypertonic saline followed 180 min later by a second injection of normal or hypertonic saline and sacrificed 30 min later. When both injections were hypertonic saline (H-H), AVP1 levels were greater than levels seen after a single hypertonic saline injection, or after an injection of normal saline followed by a second injection of hypertonic saline (N-H). This study shows acute, repeated exposure to hypertonic saline causes a robust increase in vasopressin gene transcription. Since a second hyperosmotic stimulus is known to increase neuronal firing rate and activity, our results suggest that a correlation exists with intracellular mechanisms regulating vasopressin gene transcription.

Topics: Acute Disease; Animals; Arginine Vasopressin; Male; Osmotic Pressure; Rats; Rats, Long-Evans; RNA, Heterogeneous Nuclear; Saline Solution, Hypertonic; Sodium Chloride; Stress, Physiological; Transcription, Genetic; Vasopressins

To study the physiological mechanisms of plasma hypoosmolality in patients with pneumonia and on this basis to elaborate principles of therapy for this condition.. 52 individuals of different age, including 26 patients with pneumonia, were examined. Osmolality, the concentrations of ions of sodium, potassium, magnesium, and creatinine were measured in the serum.. The patients with pneumonia were found to have osmolality, hyponatremia in combination with severe hypodiuresis, high urinary osmotic pressure and intensive reabsorption of osmotically free water in the kidney, which leads to blood dilution. As hypoosmolality usually causes higher diuresis and decreased urinary osmolality; hypodiuresis with high urinary osmolality in pneumonia is indicative of effective renal performance and its altered regulation evidently due to the hypersecretion of vasopressin or to the decreased formation of a number of autacoids in the kidney.. Blood hypoosmolality and hyponatremia in the examined patients result from inadequate blood osmolality and high urinary osmotic concentrating. The principles of this condition in pneumonia are discussed and aquaretics are proposed for use as pathogenetic therapy.

Topics: Acute Disease; Adolescent; Adult; Convalescence; Female; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Pneumonia; Vasopressins

Although it is established that the fetus can successfully withstand a single, acute hypoxaemic challenge during gestation, little is known about what effects prevailing adverse intrauterine conditions might have on the fetal response to acute hypoxaemia. The aims of this study were therefore: (1) to characterise the effects of prevailing and sustained hypoxaemia, acidaemia or hypoglycaemia on the fetal cardiovascular responses to an episode of acute hypoxaemia; and (2) to determine the effects of these adverse intrauterine conditions on mechanisms mediating these cardiovascular responses. Thirty-three Welsh Mountain sheep fetuses were chronically instrumented (1-2 % halothane) between 117 and 125 days of gestation (term is ca 145 days) with amniotic and vascular catheters and with a transit-time flow probe around a femoral artery. The animals were divided retrospectively into four groups based upon post-surgical, sustained, basal blood oxygen (chronically hypoxaemic; P(a,O2), 17.3 +/- 0.5 mmHg; n = 8), glucose (chronically hypoglycaemic; blood glucose, 0.49 +/- 0.03 mmol l(-1); n = 6) and acid-base (chronically acidaemic; pH(a), 7.25 +/- 0.01; n = 5) status. Values for compromised fetuses were -2 S.D. from a group of control (n = 14) fetuses. At 130 +/- 4 days, a 1 h episode of acute, isocapnic hypoxaemia (9 % O(2) in N(2), to reduce carotid P(a,O2) to 12 +/- 1 mmHg) was induced in all fetuses by reducing the maternal inspired O(2) fraction (F(I,O2)). Fetal cardiovascular variables were recorded at 1 s intervals throughout the experimental protocol and arterial blood samples taken at appropriate intervals for biophysical (blood gases, glucose, lactate) and endocrine (catecholamines, vasopressin, cortisol, ACTH) measures. During acute hypoxaemia all fetuses elicited hypertension, bradycardia and femoral vasoconstriction. However, prevailing fetal compromise altered the cardiovascular and endocrine responses to a further episode of acute hypoxaemia, including: (1) enhanced pressor and femoral vasoconstriction; (2) greater increments in plasma noradrenaline and vasopressin during hypoxaemia; and (3) basal upward resetting of hypothalamic-pituitary-adrenal axis function. Only chronically hypoxaemic fetuses had significantly elevated basal concentrations of noradrenaline and enhanced chemoreflex function during acute hypoxaemia. These data show that prevailing adverse intrauterine conditions alter the capacity of the fetus to respond to a subsequent episode o

Topics: Acid-Base Equilibrium; Acidosis; Acute Disease; Adrenocorticotropic Hormone; Animals; Blood Gas Analysis; Blood Glucose; Cardiovascular System; Catecholamines; Chemoreceptor Cells; Endocrine System; Female; Fetal Diseases; Fetus; Hemoglobins; Hindlimb; Hydrocortisone; Hydrogen-Ion Concentration; Hypoglycemia; Hypoxia; Lactic Acid; Pregnancy; Sheep; Vascular Resistance; Vasopressins

Hyponatremia is a well known complication of traumatic and nontraumatic cerebral injury, often related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Nonetheless, it also can be associated with a different entity, the syndrome of cerebral salt wasting (CSW). The authors report the case of a 4.5-year-old boy presenting with major head injury who at day 6 after admission had generalized tonic-clonic seizures caused by severe acute hyponatremia (serum sodium level, 119 mmol/L) and signs of dehydration. Despite initial isotonic rehydration, hyponatremia persisted because of excessive renal salt losses and concomitant enormous water losses, necessitating increasing amounts of sodium, up to 160 mmol/kg/d, and large amounts of intravenous fluids, up to 27 L/d. Highly increased levels of atrial natriuretic peptide (ANP) confirmed the diagnosis of CSW. The occurrence of a CSW has to be recognized early in the clinical course for adequate treatment and remains one of the important differential diagnosis of SIADH in hyponatremic states in patients with cerebral disorders, especially after head injury.

Topics: Acute Disease; Adrenocorticotropic Hormone; Aldosterone; Atrial Natriuretic Factor; Brain; Brain Injuries; Child, Preschool; Humans; Hydrocortisone; Hyponatremia; Male; Sodium; Vasopressins

Status epilepticus causes significant morbidity and mortality. A case of generalized status epilepticus followed by massive pulmonary aspiration, acute respiratory failure and transient central diabetes insipidus is presented. Seizures were promptly controlled, but the patient required mechanical ventilation and correction of polyuria with desmopressin acetate. During hospitalization mental status improved, diabetes insipidus spontaneously remitted and he was discharged without neurologic sequelae. The clinical and pathophysiological features of this case are discussed.

Topics: Acute Disease; Adult; Diabetes Insipidus; Humans; Male; Pneumonia, Aspiration; Respiratory Insufficiency; Status Epilepticus; Vasopressins

Topics: Acute Disease; Aquaporins; Brain Edema; Chronic Disease; Humans; Hyponatremia; Hypovolemia; Vasopressins; Water-Electrolyte Imbalance

Initial morphological and cytochemical cardiomyocyte alterations were studied at experimental acute coronary failure by histological, electron microscopy and electron histochemical methods. The results obtained demonstrated that transition of contractile myocardium to emergency function occurring at experimental conditions is accompanied by a strict rise of structural and functional heterogeneity. Prior to this process a functional and conformational unification of mitochondria takes place, passing to progress of pathological process, destructive changes of organellae causing cell death. Appearance of cellular insufficiency is acting upon all energy dependent processes: contractile cycle efficiency, function of calcium transferring systems Ca-binding sarcoplasmic reticulum function and that of mitochondria, as well efficiency of regenerative mechanisms. In appearing condition ruining of every cardiomyocyte system is possible.

Topics: Acute Disease; Animals; Coronary Disease; Disease Models, Animal; Histocytochemistry; Microscopy, Electron; Myocardium; Rabbits; Time Factors; Vasoconstrictor Agents; Vasopressins

To determine condition and adaptive capacity of cell nucleoli at ageing, the effect of acute immobilization on the hypothalamic neurosecretory cells was investigated in young and old male Wistar rats. Using immunohistochemical methods and nucleolometry we have shown that: 1) the nuclear volume in all neurosecretory cells is increased; 2) the share of cells, containing nucleoli with marginal position or multiple nucleoli in the nuclei, displays opposite changes in young and in old rats under stress condition. We suppose that adaptive mechanisms are different in young and old animals. Although, both kinds of morphological reorganization result in the increase in functional activity.

Topics: Acute Disease; Aging; Animals; Cell Count; Cell Nucleolus; Hypothalamus; Immobilization; Male; Neurosecretory Systems; Oxytocin; Rats; Rats, Wistar; Stress, Physiological; Vasopressins

Hyponatremia after subarachnoid hemorrhage (SAH) is commonly associated with diuresis and natriuresis, but the causes are still controversial. We investigated whether brain natriuretic peptide (BNP) was related to such hyponatremia.. Plasma BNP concentrations were measured by immunoradiometric assay in 18 patients at 0 to 2 days (period 1), 7 to 9 days (period 2), and > 14 days (period 3) after SAH. Plasma concentrations of antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and noradrenaline were also measured during period 2.. The 11 patients with hyponatremia (serum sodium concentration of < 135 mEq/L) had much higher plasma BNP concentrations during each period than did healthy controls (P < 0.05), whereas the 7 patients with normonatremia did not show statistically higher values. In the patients with hyponatremia, the plasma BNP concentration during period 2 was statistically higher than that during periods 1 and 3 (P < 0.05). The plasma noradrenaline concentration during period 2 was higher in patients with hyponatremia than in those with normonatremia (P < 0.05), whereas the plasma concentrations of ADH and ANP during period 2 were not statistically different between the hyponatremic and normonatremic patients.. We conclude that BNP may be related to hyponatremia associated with natriuresis following SAH. The increase of noradrenaline may promote the secretion of BNP.

Topics: Acute Disease; Aged; Female; Humans; Hyponatremia; Male; Middle Aged; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Norepinephrine; Radioimmunoassay; Sodium; Subarachnoid Hemorrhage; Vasopressins

Substance P receptor-like immunoreactive (SPR-LI) structures and changes following intravenous injection of vasopressin in the medullary visceral zone (MVZ) of the rat were studied by using immunohistochemical methods. In normal control rats the distribution of SPR-LI structure in MVZ generally matched with that of immunostaining against substance P (SP-LI) except in some areas. SPR-LI neurons and dendrites differed in size and shape in different areas of MVZ. Their dendrites could be classified into three types, i.e, wool-shaped, smooth and varicose. Some SPR-LI neurons were also positive for tyrosine hydroxylase-like immunoreactivity (TH-LI) . After administration of vasopressin SPR-LI structures became denser, especially at levels of pyramidal decussation (PYX) and area postrema (AP). The dendrites of motor dorsal nucleus of X (NMDX) in the dorsal part of MVZ appeared thin and straight in morphology instead of curl and thick outlooks. These results implicate that some SPR-LI neurons might be involved in the modulation of the cardiovascular stress induced by vasopressin.

Topics: Acute Disease; Animals; Immunohistochemistry; Injections, Intravenous; Male; Medulla Oblongata; Myocardial Ischemia; Rats; Rats, Sprague-Dawley; Receptors, Neurokinin-1; Tyrosine 3-Monooxygenase; Vasopressins

For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations.. Matched polydipsic schizophrenic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours.. Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients (P < .02), despite their consistently lower plasma osmolality (P < .007). No known or putative antidiuretic hormone stimulus could account for this finding. Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated with the peak antidiuretic hormone responses, but neither factor could explain the difference in the response by the 2 groups.. Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at increased risk of life-threatening water intoxication.

Topics: Acute Disease; Adult; Arginine Vasopressin; Blood Pressure; Drinking; Female; Heart Rate; Humans; Hydrocortisone; Hyponatremia; Inappropriate ADH Syndrome; Male; Methylphenidate; Osmolar Concentration; Psychiatric Status Rating Scales; Schizophrenia; Schizophrenic Psychology; Sodium; Thirst; Vasopressins; Water Intoxication

Recently, we demonstrated that elevated blood pressure activates mitogen-activated protein (MAP) kinases in rat aorta. Here we provide evidence that the vascular response to acute hypertension also includes induction of MAP kinase phosphatase-1 (MKP-1), which has been shown to function in the dephosphorylation and inactivation of MAP kinases. Restraint or immobilization stress, which leads to a rapid rise in blood pressure, resulted in a rapid and transient induction of MKP-1 mRNA followed by elevated MKP-1 protein expression in rat aorta. That the induction of MKP-1 by restraint was due to the rise in blood pressure was supported by the finding that several different hypertensive agents (phenylephrine, vasopressin, and angiotensin II) were likewise capable of eliciting the response, and sodium nitroprusside, a nonspecific vasodilator agent that prevented the acute rise in blood pressure in response to the hypertensive agents, abrogated MKP-1 mRNA induction. The in vivo effects could not be mimicked by treatment of cultured aortic smooth muscle cells with similar doses of the hypertensive agents. These findings support a role for MKP-1 in the in vivo regulation of MAP kinase activity during hemodynamic stress.

Topics: Acute Disease; Angiotensin II; Animals; Antihypertensive Agents; Blood Pressure; Blotting, Western; Cardiovascular System; Cells, Cultured; Data Interpretation, Statistical; Enzyme Activation; Gene Expression Regulation, Enzymologic; Hypertension; Male; Mitogens; Muscle, Smooth, Vascular; Nitroprusside; Phenylephrine; Phosphoprotein Phosphatases; Protein Kinases; Protein Phosphatase 1; Rats; Rats, Wistar; Restraint, Physical; RNA; Stress, Physiological; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

This study, the first using the pig, examined expression of mRNAs for vasopressin (VP), oxytocin (OT), preproenkephalin (PENK) and pro-opiomelanocortin (POMC) in the forebrain, and of POMC and prolactin in the pituitary. High basal expression of VP and OT mRNAs was present in the paraventricular (PVN) and supraoptic (SON) nuclei. In the PVN, VP was found in magnocellular regions whereas OT was also seen in the parvocellular portion; the distribution of VP and OT mRNAs in the SON was as reported in other species. The suprachiasmatic nucleus contained VP mRNA but only OT message was present in the dorsomedial SON, a structure peculiar to swine. Gene expression for PENK occurred in the caudate putamen (CPu), for POMC in the mediobasal hypothalamus (MBH) and for prolactin and POMC in the hypophysis. Following restraint, VP message increased in the magnocellular PVN, as did PENK in the CPu and POMC in the MBH.

Topics: Acute Disease; Animals; Basal Metabolism; Enkephalins; Gene Expression; Hypothalamus; Male; Oxytocin; Pituitary Gland; Pro-Opiomelanocortin; Prolactin; Prosencephalon; Protein Precursors; Restraint, Physical; Stress, Physiological; Swine; Vasopressins

Vasovagal reflexes, such as hypotension and bradycardia, are induced by rapid hemorrhage and mimic neurocardiogenic reflexes in mammals. We examined the role of vasopressin in the neurocardiogenic responses to mild, rapid hemorrhage (1 mL/100 g for 30 seconds) and severe hemorrhage (1 mL/100 g body wt for 30 seconds repeated three times at 11-minute intervals) in homozygous Brattleboro and Long-Evans rats. Mild, rapid hemorrhage induced severe bradycardia and hypotension only in Long-Evans rats. Exogenous vasopressin (1.85 pmol/kg per minute for 1 hour) restored both the bradycardic and hypotensive responses in Brattleboro rats. DDAVP, a vasopressin V2-receptor agonist (0.19 pmol/kg per minute for 24 hours), did not affect the cardiovascular responses to hemorrhage in Brattleboro rats, although it maintained urine production within normal limits. However, OPC-31260 (21.6 mumol/kg IV), a vasopressin V2-receptor antagonist, attenuated both the hypotensive and bradycardic responses to hemorrhage in Long-Evans rats. A vasopressin V1-receptor antagonist attenuated bradycardia and delayed the recovery of arterial pressure after hemorrhage but did not affect the hypotension that occurred immediately after hemorrhage in Long-Evans rats. Methylatropine also attenuated both the bradycardic and hypotensive responses induced by hemorrhage, but propranolol had no effect on the cardiovascular responses to hemorrhage in Long-Evans rats. The recovery of arterial pressure after repeated hemorrhage was less adequate in Brattleboro rats than in Long-Evans rats. Our results suggest that the neurocardiogenic responses to hemorrhage, especially hypotension, may be related to vasodilation induced by a V2-receptor-mediated mechanism and by the vagal reflex, both of which are substantiated by the existence of vasopressin. The coexistence of V1- and V2-receptor mechanisms may be necessary for the hypotensive response to hemorrhage. We found that a V2-receptor antagonist attenuated the hypotension mediated by the so-called neurocardiogenic reflex.

Topics: Acute Disease; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Autonomic Nerve Block; Benzazepines; Cardiovascular System; Deamino Arginine Vasopressin; Diabetes Insipidus; Heart; Hemorrhage; Male; Nervous System; Rats; Rats, Brattleboro; Rats, Inbred Strains; Receptors, Vasopressin; Recurrence; Vasopressins

A 35-year-old male sustained a full-skin thickness chemical burn involving 60 per cent of TBSA when hydrochloric acid was applied to his face, trunk and extremities by his girlfriend. Debridements and skin graftings were performed smoothly and he was doing well until day 23 after injury, when massive GI tract bleeding caused a drop in blood pressure. Vasopressin was given intravenously to control the bleeding, which stopped, and the blood pressure returned to normal after transfusion. After the vasopressin infusion was tapered off acute pulmonary oedema developed abruptly, which required treatment by intubation and PEEP using a respirator. The lung condition had returned to normal by the following day. A second episode of massive GI tract bleeding recurred 10 days later, again vasopressin was given through a catheter into the inferior mesenteric artery. Again pulmonary oedema developed 38 h after the vasopressin use, the oedema disappeared within 2 days when the vasopressin infusion tapered off. It should be kept in mind that acute pulmonary oedema may develop when high doses of vasopressin are used in the treatment of Curling's ulcer or other GI tract bleeding.

Topics: Acute Disease; Adult; Burns, Chemical; Debridement; Gastrointestinal Hemorrhage; Hemostatics; Humans; Infusions, Intravenous; Male; Pulmonary Edema; Radiography, Thoracic; Skin; Skin Transplantation; Vasopressins

Bleeding from oesophageal varices is an uncommon but potentially fatal condition that often leads to expensive hospitalizations in intensive care or high-dependency units.. To assess the clinical and economic impact of this condition, we have devised a management plan illustrating current clinical practice in the UK.. Approximately 6.1 million pounds of NHS resources are devoted to the treatment of 3000 acute hospital admissions for variceal bleeding every year. Vasoconstrictors like vasopressin may save approximately 36 lives per annum for an additional 145 thousand pounds. However, current clinical practice requires vasopressin to be concurrently administered with intravenous glyceryl trinitrate, increasing overall costs by 582 thousand pounds to a total of 6.7 million pounds. The additional cost for each extra life saved is estimated at 16,180 pounds.. The efficacy of current vasoconstrictors requires further confirmation. In particular, new agents like octreotide (Sandostatin) should be carefully assessed to determine their potential clinical and economic benefits.

Topics: Acute Disease; Costs and Cost Analysis; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hospitalization; Humans; Nitroglycerin; Patient Care Planning; United Kingdom; Vasoconstrictor Agents; Vasopressins

Hemorrhage induces a rapid redistribution of protein from extravascular spaces into the blood. We studied the effects of acute, nontraumatic hemorrhage on tracer-albumin clearances into individual tissues of rats to determine if reduced protein extravasation could account for intravascular protein gain. Three groups were studied: 1) HEM animals were anesthetized with pentobarbital sodium and bled to a mean arterial pressure of 50 mmHg for 90 min; 2) HEM-RS animals were treated identical to group 1 and then resuscitated with 5% bovine serum albumin (BSA) until baseline arterial pressures were regained; 3) SHAM animals served as time controls. Hemodynamic variables were measured periodically throughout hemorrhage and clearance periods, and plasma samples were collected prior to death for protein and hormone analysis. Plasma clearance of 131I-BSA into individual tissues was measured over the final 30 min of each protocol with a terminal injection of 125I-BSA used to correct for intravascular volume. Reduction of blood volume by 35% in HEM-treated animals resulted in a marked decrease in albumin transport relative to the SHAM group (p < or = .05) in the following tissues: skeletal muscle (-65%), skin (-49%), ileum (-75%), cecum (-66%), colon (-67%), heart (-67%), and lung (-71%). Significant changes were not observed in the remaining tissues sampled: pancreas, kidney, and cerebrum. Albumin clearances in the HEM-RS group were slightly but not significantly lower than SHAM animals except for skeletal muscle, where transport remained depressed following resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Animals; Atrial Natriuretic Factor; Biological Transport; Blood Glucose; Blood Volume; Body Water; Body Weight; Brain; Colon; Coronary Vessels; Disease Models, Animal; Extravascular Lung Water; Hematocrit; Hemodynamics; Hemorrhage; Ileum; Lung; Male; Osmolar Concentration; Plasma Volume; Rats; Rats, Wistar; Resuscitation; Serum Albumin; Skin; Tissue Distribution; Vasopressins

Topics: Acute Disease; Aldosterone; Animals; Calcium; Cochlear Duct; Humans; Hyaluronic Acid; Hyaluronoglucosaminidase; Meniere Disease; Sodium; Vasopressins

Topics: Acute Disease; Esophageal and Gastric Varices; Esophagoscopy; Gastrointestinal Hemorrhage; Humans; Octreotide; Sclerotherapy; Somatostatin; Vasopressins

The present study was designed to investigate the effect of a lack of vasopressin resulting from electrolytic lesion of the median eminence of the hypothalamus on the acute 45-min aortic coarctation hypertension elicited in conscious rats by means of a pneumatic cuff placed around the aorta above the renal arteries. Forty-eight hours after lesion, aortic constriction elicited a prompt (5-min) rise in mean carotid pressure from 115 +/- 2 to 149 +/- 2 mmHg, followed by a gradual decline to 129 +/- 2 mmHg. In contrast, sham-lesioned rats exhibited a prompt hypertensive response from 118 +/- 2 to 157 +/- 2 mmHg that leveled off throughout the experiment. Lesioned rats treated with saralasin presented a blunted hypertensive response (within 125 +/- 2 to 130 +/- 2 mmHg), whereas sham-lesioned rats showed only a delay in the onset of hypertension. The hypertensive response of lesioned rats was unaffected by the vasopressin antagonist [d(CH2)5Tyr(Me)]AVP, whereas sham-lesioned rats submitted to this treatment presented a prompt rise in pressure followed by a gradual decline at the end of the experiment. Lesioned and sham-lesioned rats treated with saralasin plus vasopressin antagonist showed a blunted hypertensive response throughout the experiment. These data demonstrate that the integrity of the median eminence plays a pivotal role in the maintenance (30-45 min) of acute aortic coarctation hypertension, presumably involving the release of vasopressin from the neurohypophysis, whereas angiotensin II mainly accounts for the prompt (5-15 min) rise in pressure.

Topics: Acute Disease; Animals; Aortic Coarctation; Arginine Vasopressin; Blood Pressure; Hypertension; Male; Median Eminence; Rats; Rats, Wistar; Saralasin; Vasopressins

Subcutaneous injection of the potent, nonselective opioid antagonist diprenorphine inhibits the vasopressin response to acute hypovolemia. To determine if this inhibition is due to antagonism of opioid receptors in brain pathways that mediate volume control, we determined the vasopressin response to different stimuli when diprenorphine or other opiates were injected into the cerebral ventricles, the nucleus tractus solitarius (NTS), or the lateral parabrachial nucleus (PBN) of rats. We found that the vasopressin response to hypovolemia was inhibited by injection of diprenorphine into the cerebral ventricles at a dose too low to be effective when given subcutaneously. This response also was inhibited when a 20-fold lower dose of diprenorphine was injected into the PBN but not when it was injected into the NTS. The inhibitory effect of diprenorphine in the PBN was not attributable to a decrease in osmotic or hypovolemic stimulation and did not occur with osmotic or hypotensive stimuli. Injecting the PBN with equimolar doses of the mu antagonist naloxone, the delta antagonist ICI-154,129 or the kappa-1 agonist U-50,488H had no effect on basal or volume-stimulated vasopressin. We conclude that the inhibition of vasopressin by diprenorphine is due partially to action at a novel class of opioid receptors that transmit volume stimuli through the PBN.

Topics: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Acute Disease; Animals; Antihypertensive Agents; Brain; Cerebral Ventricles; Diprenorphine; Enkephalin, Leucine; Hemodynamics; Male; Naloxone; Narcotic Antagonists; Pyrrolidines; Rats; Rats, Sprague-Dawley; Shock; Solitary Nucleus; Stimulation, Chemical; Vasopressins

The experiments were designed to determine whether potassium-loaded rats have a deficient recovery of blood pressure after a rapid arterial haemorrhage. Potassium loading was achieved by providing a 0.75% KCl solution as drinking fluid for 14 days, while control rats had either distilled water or tapwater. MAP, HR, Hct, and plasma electrolytes were determined before and after 1 and 2% body weight haemorrhage in anaesthetized Sprague-Dawley rats. Potassium-loaded rats had significantly reduced blood pressure recovery within 20 min after haemorrhage. HR was significantly reduced within 5 min only after 2% haemorrhage in potassium-adapted rats. Haemorrhage induced significant hyperkalaemia which was greater and significantly prolonged after 2% haemorrhage. The significant fall in Hct after haemorrhage was not affected by the magnitude of haemorrhage. In an additional group of rats, the pressor response to intravenous infusion of vasopressin was unaffected by potassium loading, whereas that to noradrenaline and angiotensin II was significantly reduced throughout the 20 min of infusion. The peak increase in blood pressure after phenylephrine injection was, however, unaffected by potassium loading. Basal plasma catecholamines concentration as well as concentrations after 1% haemorrhage were unaffected by potassium loading. It is concluded that the reduced vascular response to noradrenaline and angiotensin contributed to the reduced recovery of blood pressure after haemorrhage in potassium-loaded rats. Furthermore, the result with phenylephrine suggest a mechanism that is unrelated to direct vascular effects of noradrenaline and angiotensin II.

Topics: Acute Disease; Adaptation, Physiological; Anesthesia; Angiotensin II; Animals; Blood Pressure; Cardiovascular Physiological Phenomena; Catecholamines; Hemodynamics; Hemorrhage; Infusions, Intravenous; Male; Norepinephrine; Potassium; Rats; Rats, Sprague-Dawley; Vasopressins

The hemodynamic effect of combined V2/V1 arginine vasopressin (AVP) antagonist in conscious rats with acute 24 hour streptozotocin (STZ)--induced diabetes was studied using the microsphere technique. The rats were made diabetic with a single intravenous injection of STZ (60 mg/kg). One day after STZ administration the hemodynamic parameters in the experimental animals were measured before and 10 minutes after AVP antagonist injection (50 mg/kg, i.v.). The hemodynamic alterations observed post-antagonist included: 1) an increase in the total peripheral resistance (1.84 +/- 0.15 vs. 1.31 +/- 0.12 mm Hg/ml/min per 100 g before antagonist administration, p < 0.05), 2) a decrease in the cardiac index (49.0 +/- 3.1 vs. 68.7 +/- 5.2 ml/min/100 g before antagonist administration, p < 0.05) and stroke volume (0.40 +/- 0.03 vs. 0.57 +/- 0.06 ml before antagonist administration, p < 0.05), 3) a significant (p < 0.05) decrease in the blood flow to the skin, skeletal muscle, stomach, small intestine and kidneys. The mean arterial pressure and heart rate remained unchangeable post-antagonist. These data suggest that AVP is responsible, at least in part, for prominent hemodynamic alterations observed in conscious rats with 24 hour STZ-induced diabetes.

Topics: Acute Disease; Animals; Arginine Vasopressin; Diabetes Mellitus, Experimental; Hemodynamics; Male; Rats; Receptors, Vasopressin; Time Factors; Vasopressins; Wakefulness

Cholestatic patients undergoing surgery have increased mortality and demonstrate clinical features suggestive of adrenal insufficiency. To examine whether cholestasis influences the status of the hypothalamic-pituitary-adrenal axis, we evaluated rats with acute cholestasis caused by bile duct resection (BDR) and sham-operated and unoperated controls. Basal unstressed plasma concentrations of ACTH and corticosterone were similar in BDR and sham-operated and unoperated control rats. However, exposure of BDR rats to saturated ether vapor resulted in significantly less ACTH and corticosterone release in plasma than in the control animals. To understand the mechanism(s) of decreased HPA axis responsiveness to ether stress in cholestasis, we administered corticotropin-releasing factor (CRF) and measured hypothalamic content, mRNA levels and in vitro secretion of CRF and arginine vasopressin (AVP), the two principal secretagogues of ACTH. In BDR animals, ACTH responses to CRF were decreased and hypothalamic content of CRF and CRF mRNA expression in the paraventricular nucleus were decreased by 25 and 37%, respectively. Furthermore, CRF release from hypothalamic explants of BDR rats was 23% less than that of controls. In contrast to CRF, hypothalamic content of AVP was 35% higher, AVP mRNA in the paraventricular nucleus was increased by 6.6-fold, and hypothalamic explant release of AVP was 24% higher in BDR rats than in control animals. Pituitary ACTH contents were similar in BDR and sham resected rats, but higher than unoperated controls. These findings demonstrate that acute cholestasis in the rat is associated with suppression of hypothalamic-pituitary-adrenal axis responsiveness to stress and demonstrate a dissociation between mechanisms of ACTH regulation mediated by CRF and AVP.

Topics: Acute Disease; Adrenocorticotropic Hormone; Animals; Arginine Vasopressin; Bile Ducts; Cholestasis; Corticosterone; Corticotropin-Releasing Hormone; Ether; Hypothalamo-Hypophyseal System; Hypothalamus; Male; Organ Culture Techniques; Paraventricular Hypothalamic Nucleus; Pituitary Gland; Pituitary-Adrenal System; Rats; Rats, Sprague-Dawley; Reference Values; RNA, Messenger; Stress, Physiological; Vasopressins

The defense of brain volume during hyponatremia cannot be explained by the losses of brain sodium and potassium. We have examined the brain losses of organic osmolytes in rats after 24 h of severe hyponatremia induced by the administration of vasopressin and 5% dextrose in water. Normonatremic controls and animals with intermediate plasma sodium concentration ([Na]) were produced in vasopressin-treated animals by the administration of isocaloric gavages containing varying amounts of NaCl and free water. The animals were killed at 24 h by decapitation, and one brain hemisphere was quickly frozen in liquid nitrogen for organic osmolyte determinations. When compared with controls (plasma [Na] = 139 +/- 1.5 mM), hyponatremic animals (plasma [Na] = 96 +/- 1 mM) had significantly reduced brain contents for sodium, potassium, chloride, glutamate, myo-inositol, N-acetylaspartate, aspartate, creatine, taurine, gamma-aminobutyric acid, and phosphoethanolamine. Plasma [Na] was highly correlated (P < 0.001) with the brain contents for sodium, potassium, and organic osmolytes. Whereas the observed increase in brain water during hyponatremia was only 4.8%, by calculation, brain swelling without brain organic osmolyte losses would have been 11%, an amount that jeopardizes survival.

Topics: Acute Disease; Amino Acids; Animals; Brain; Creatine; Deamino Arginine Vasopressin; Hyponatremia; Inositol; Male; Rats; Rats, Sprague-Dawley; Vasopressins

In normal anaesthetized rats (pentobarbital, 40 mg/kg i.p.), intravenous injection of a bolus of vasopressin (0.3 micrograms/kg) provoked a large increase in pulmonary and in systemic blood pressures. About three minutes later, some rats (60%) developed an acute pulmonary edema (OPA), froth appearing at the trachea. Other animals presented no OPA at the 4th minute following the injection, but OPA appeared immediately when bilateral vagotomy was performed at that time. Factors explaining the appearance of OPA are mechanical ones, circulatory or respiratory, without interferences with autonomous nervous processes.

Topics: Acute Disease; Animals; Disease Models, Animal; Hemodynamics; Pulmonary Edema; Rats; Rats, Inbred Strains; Vasopressins

The systemic and regional hemodynamic effects of arginine vasopressin receptor antagonism (AVPA) and angiotensin-converting enzyme inhibition (ACEi) were examined in rabbits with acute left ventricular failure induced by repetitive direct current (DC) shock. Hemodynamic measurements in 24 rabbits 24 h after DC shock compared with 6 sham-operated controls demonstrated a lowered cardiac output (602 +/- 26 vs. 920 +/- 35 ml/min, P less than 0.01), increased left ventricular end-diastolic pressure (LVEDP, 13.6 +/- 1.3 vs. 1.9 +/- 0.5 mmHg, P less than 0.01) and a raised peripheral resistance (9,734 +/- 495 vs. 6,479 +/- 305 dyn.s.cm-5, P less than 0.01). Cerebral blood flow was not altered in rabbits with acute left ventricular failure but intestinal (29 +/- 2 vs. 53 +/- 9 ml/min, P less than 0.01) and renal (82 +/- 6 vs. 130 +/- 8 ml/min, P less than 0.01) blood flows were significantly reduced. No hemodynamic changes were observed after AVPA alone in the acute heart failure group and ACEi alone reduced LVEDP and increased renal vascular conductance. Treatment with both drugs (i.e., AVPA + ACEi) resulted in a significant increase in cardiac output (21%) and a decrease in blood pressure (19%) and peripheral resistance (34%) and restored renal and intestinal blood flows to near normal levels. Thus both vasopressin and angiotensin contribute to the overall increase in peripheral resistance in this model and to the decrease in intestinal and renal blood flow observed. Presumably blockade of one system produced little hemodynamic change because of compensatory increases in the other system.

Topics: Acute Disease; Angiotensin II; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Arginine Vasopressin; Blood Pressure; Cardiac Output, Low; Electroshock; Female; Heart Ventricles; Hemodynamics; Hormones; Male; Rabbits; Receptors, Vasopressin; Regional Blood Flow; Vasopressins

A study of neurohumoral and functional determinants of the advance of Ischemic heart disease in 39 patients with unstable stenocardia with positive results of loading tests (transesophageal electrocardiostimulation and veloergometry) allowed to reveal a significant reduction of the coronary reserve and regional dysfunction of the myocardium that interrelated with changes of the prostacyclin/thromboxane balance, increase of vasopressin with unchanged angiotensin II value and increased marker of the functional state of thrombocytes--beta-thromboglobulin. These changes may be one of the leading links in the pathogenesis of destabilization.

Topics: Acute Disease; Angiotensin II; beta-Thromboglobulin; Coronary Disease; Epoprostenol; Fibrinopeptide A; Humans; Physical Exertion; Radioimmunoassay; Thromboxane A2; Vasopressins

No study has, to our knowledge, evaluated the acute effects of low immunosuppressive doses of cyclosporin (CsA) on renal function. To establish whether a relationship exists between the dosage of CsA and the onset of nephrotoxicity, 28 rats were studied by renal clearances before (control) and after i.v. administration of different doses of CsA: 3 mg/kg b.w. (group 1); 7 mg/kg b.w. (group 2); 11 mg/kg b.w. (group 3); 15 mg/kg b.w. (group 4). No change in renal function was observed between control and the post-CsA period in groups 1 and 2. GFR (inulin clearance) was decreased vs the control period in group 3 and group 4 (-22% and -37%, respectively, P less than 0.001); the difference between these two groups was statistically significant (P less than 0.01). Effective renal plasma flow (PAH clearance) was similarly decreased in groups 3 and 4 vs their control periods (-21% and -28%, respectively, P less than 0.001) due to the increase of total renal vascular resistance (+41% and +42%, respectively, P less than 0.001). Filtration fraction was significantly decreased by CsA in group 4 (P less than 0.01 vs the control period). PAH renal extraction, urinary volume, and sodium and potassium excretion were similar in all groups before and after CsA. PRA and ADH were significantly increased only in group 4 (P less than 0.01) vs the baseline values. A high and significant relationship was detected between CsA dosage and the decrease of GFR (r = 0.81, P less than 0.001) and RPF (r = 0.612, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Animals; Blood Pressure; Body Weight; Cyclosporins; Glomerular Filtration Rate; Hematocrit; Kidney Diseases; Male; Potassium; Rats; Rats, Inbred Strains; Renal Circulation; Sodium; Vasopressins

This "syndrome" has been observed in 4 of 23,935 in-patients registered in the years 1974-1987 in the Comprehensive Hospital Drug Monitoring (Bern/St. Gallen), with 6 reactions. Signs of an attack of bronchial asthma, laryngeal or pulmonary edema or a (heart-)circulatory event were not observed. Each patient was cyanotic and 3 had the feeling of impending death. The eliciting drugs were penicillin-G (twice) and cefazolin (once), given i.v.; iron dextran i.m. (once); pitressin tannate i.m. (once) and dicobalt edetate (Kelocyanor) i.v.(once). In each case the reaction started during or shortly after injection of the drug; the duration of the reaction in 5 of these events was 20-80 minutes. The pathomechanism could be a special form of anaphylactic reaction with acute pulmonary hypertension, comparable to IgE-induced anaphylaxis in the rabbit or aggregate anaphylaxis in the monkey or the dog. Further observations are needed for more detailed study.

Topics: Acute Disease; Adult; Arginine Vasopressin; Cefazolin; Chelating Agents; Cyanosis; Drug-Related Side Effects and Adverse Reactions; Dyspnea; Edetic Acid; Female; Humans; Iron-Dextran Complex; Male; Middle Aged; Penicillin G; Vasopressins

Advances in endoscopic therapy have dramatically altered the approach to acute upper gastrointestinal tract hemorrhage. It can no longer be assumed that early endoscopic evaluation of this condition does not affect outcome. In the management of selected patients with nonvariceal hemorrhage, endoscopic therapy affects rates of rebleeding, need for surgery and transfusions, and length of hospitalization. For patients with variceal hemorrhage, the impact of endoscopic treatment is less clear. The endoscopic advances of the past decade have been exciting and have presented new challenges. Future investigators need to better define subgroups of patients who will benefit from this technology and determine which of the many techniques available will be safest and most efficacious.

Topics: Acute Disease; Endoscopy; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Laser Therapy; Peptic Ulcer Hemorrhage; Recurrence; Sclerotherapy; Vasopressins

The aim of this paper was to study atrial natriuretic factor, plasma renin activity and antidiuretic hormone values during paroxysmal atrial arrhythmias with different ventricular rates before and after pharmacological cardioversion and during chronic atrial flutter-fibrillation. The study was carried out: 1) during acute arrhythmias (atrial flutter-fibrillation or supraventricular tachycardia) and after restoration of normal sinus rhythm in 2 patients without heart disease, in 13 with chronic heart disease and in 6 with acute myocardial infarction; 2) during chronic atrial flutter-fibrillation in 5 patients with chronic ischemic heart disease, without congestive heart failure. Atrial natriuretic factor, aldosterone, plasma renin activity and antidiuretic hormone values were measured by radio-immunoassay. During paroxysmal atrial arrhythmias atrial natriuretic factor levels were higher than normal in all patients, particularly in those with supraventricular tachycardia. Most of the aldosterone measurements were above the normal range. As far as plasma renin activity and antidiuretic hormone values are concerned, levels higher than the normal range were found in the patients with severe hemodynamic impairment. Central venous pressure was above normal in all patients except in the 2 without heart disease, and there was a positive correlation between atrial natriuretic factor and central venous pressure values. After restoration of normal sinus rhythm atrial natriuretic factor values returned to normal except in acute myocardial infarction patients, in 1 chronic ischemic heart disease patient with congestive heart failure and in 3 patients with mitral valve disease. In all patients with chronic atrial flutter-fibrillation and in 5 patients with acute atrial flutter-fibrillation and low rate, above normal atrial natriuretic factor values were found with normal central venous pressure values. Atrial distension due to high central venous pressure values, lack of atrial contraction and rhythmic detension of the atrial stretch receptors, may be considered the major stimuli responsible for atrial natriuretic factor release during acute paroxysmal atrial arrhythmias and atrial flutter-fibrillation with low ventricular rate, respectively.

Topics: Acute Disease; Adult; Aged; Aldosterone; Atrial Fibrillation; Atrial Flutter; Atrial Natriuretic Factor; Blood Pressure; Central Venous Pressure; Chronic Disease; Female; Humans; Male; Middle Aged; Renin; Tachycardia, Supraventricular; Vasopressins

Isolated ultrafiltration was performed in 107 patients with refractory heart failure (HF) which developed in the presence of different cardiovascular diseases. The beneficial action of isolated ultrafiltration in 71 patients (68%) with refractory HF was determined by complex interaction of the effects provoked by ultrafiltrate removal. Among those effects of paramount importance was correction of secondary hyperaldosteronism and reduction of the concentration of antidiuretic hormone accompanied by the improvement of liver and heart functions.

Topics: Acute Disease; Adult; Aged; Diuresis; Heart Failure; Hemofiltration; Humans; Middle Aged; Renin-Angiotensin System; Vasopressins

The role of vasopressin (AVP) and angiotensin II (ANG II) in the onset of acute (45 min) aortic coarctation hypertension was studied in conscious rats. Changes in mean carotid pressure (MCP) and heart rate (HR) were measured in four groups of rats. Control rats presented a hypertensive response that attained a plateau 5 min after coarctation and remained near this level throughout the experiment. Rats treated with AVP V1-vascular receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5Tyr(Me)AVP] presented a prompt rise in MCP similar to the control rats, but in contrast to this group, the MCP started to decline progressively. Rats treated with saralasin presented a delay in the onset of hypertension right after coarctation but slowly attained values similar to those for control rats. In contrast, the rats treated with AVP antagonist plus saralasin showed a blunted MCP elevation throughout the experiment. Reflex bradycardia observed in the rats treated with saralasin or the AVP antagonist plus saralasin was similar to that observed in the control rats, whereas for the group treated only with AVP antagonist, the reflex bradycardia was more intense than for the other three groups, indicating an increased sensitivity of the baroreflex. These data demonstrate that in addition to the mechanical effect of aortic constriction, both ANG II and AVP participate in the onset of acute aortic coarctation hypertension. Moreover, the results indicate that ANG II acts on the prompt (5 min) rise in pressure, whereas AVP is responsible for the maintenance (30-45 min) of the arterial pressure elevation.

Topics: Acute Disease; Angiotensin II; Animals; Aortic Coarctation; Arginine Vasopressin; Blood Pressure; Carotid Arteries; Heart Rate; Hypertension; Male; Rats; Rats, Inbred Strains; Saralasin; Vasopressins

Plasma ADH, PA and PRA in patients with respiratory failure (RF) were studied. RF patients were divided into 4 groups, i.e. acute RF (ARF) and chronic RF (CRF), with or without hypercapnia. The levels of these hormones were significantly higher in RF than those in control subjects, moreover, they were markedly elevated in ARF than those in CRF. In multiple regression analysis, ADH correlated with PaO2, pH and PRA in RF patients, but correlated with serum osmolality in control subjects. It was considered that ADH in RF was affected by the direct effect of blood gases and circulatory disorder. The mechanism of elevated PA and PRA in RF probably was mediated through restriction of intake of water and Na, reduction of renal blood flow and decreased ACE often occurred in RF. Abnormally elevated hormones are more often recognized in edematous patients than in nonedematous patients. It was suggested that many patients with RF develop heart failure or edema due to hormonal abnormalities.

Topics: Acute Disease; Aged; Aldosterone; Chronic Disease; Female; Humans; Male; Middle Aged; Renin; Respiratory Insufficiency; Vasopressins

The area postrema is a circumventricular organ that plays an important role in neurohumoral regulation of the circulation. We have developed a method to examine permeability and vascular responses of the microcirculation of the area postrema in vivo. A craniotomy was performed over the dorsal brain stem in anesthetized rats, and blood vessels to the area postrema were visualized with fluorescein microscopy. Extravasation of sodium fluorescein (MW, 386), but not 150 kDa (MW) fluorescein isothiocyanate-dextran, occurred in the area postrema under control conditions. There was no extravasation of fluorescein or dextran in the brain stem under control conditions. Acute hypertension produced marked disruption of the barrier to 150 kDa dextran in the area postrema, compared with minimal disruption in the brain stem. We tested the hypothesis that the area postrema has greater permeability to small molecules than the brain stem and that this permeability might be accompanied by distinctive vascular responses. Topical suffusion of adenosine and ADP produced similar dose-related dilation of arterioles to area postrema and dorsal brain stem. Topical and intravenous vasopressin produced similar dose-related constriction of vessels to area postrema and brain stem. Electron microscopy in rats demonstrated that a barrier to horseradish peroxidase, which is absent in capillaries in the area postrema, is present in arterioles that supply the area postrema.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Animals; Arabinose; Arterioles; Blood Vessels; Capillary Permeability; Cerebral Ventricles; Horseradish Peroxidase; Hypertension; Male; Microcirculation; Osmolar Concentration; Rats; Rats, Inbred Strains; Vasoconstriction; Vasopressins

In neurosurgical patients with hyponatraemia (plasma sodium less than 130 mmol/l) and natriuresis, increased antidiuretic hormone (ADH) secretion may be appropriate rather than inappropriate. Ten such patients were studied prospectively to assess circulating ADH concentration and body fluid volumes. Compared with a control group, the mean plasma ADH level was significantly elevated (0.9 pmol/l (s.e.m. = 0.2) versus 0.2 pmol/l (s.e.m. = 0.1], the total body water was normal (101% (s.e.m. = 3) versus 100% (s.e.m. = 6], while the blood volume was significantly reduced (89% (s.e.m. = 3) versus 104% (s.e.m. = 5]. The elevated ADH level was therefore appropriate to a reduced blood volume. This suggests that, in neurosurgical patients with hyponatraemia, fluid restriction could be dangerous. Serial observations in this small group of patients showed that salt replacement and normal fluid intake resulted in a fall in the elevated ADH levels.

Topics: Acute Disease; Adult; Blood Volume; Body Water; Brain Diseases; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Natriuresis; Plasma Volume; Prospective Studies; Vasopressins

The mechanism of hyponatremia associated with pneumonia has not been definitely established. Moreover, renal water excretion was never systematically investigated in cases of pneumonia without hyponatremia. We therefore studied nine consecutive patients breathing spontaneously (nasal oxygen in five), with acute infectious pneumonia and normal plasma sodium concentration. All the patients were previously healthy. Water loads were administered during illness and after recovery. Extracellular fluid volume, arterial blood pressure, PaO2, and PaCO2 were identical during and after pneumonia. By contrast, renal water excretion was markedly impaired during pneumonia and returned to normal values after recovery. This was attested to by a significant decrease in minimum urine osmolality together with significant increases in the percentage of the excreted water load and the maximum free water clearance, after resolution of the pneumonia. Plasma arginine vasopressin values were significantly higher during pneumonia than after recovery despite similar plasma sodium concentrations, both before and after water load. A positive correlation between plasma arginine vasopressin and minimum urine osmolality was found during pneumonia. Thus, impairment in renal water excretion appeared to be due to resetting of the vasopressin osmostat and could not be attributed to any recognized nonosmotic stimulus for vasopressin secretion. On the other hand, these defects varied in severity depending on the extent of the pneumonia and persisted until clearing of alveolar opacities, accounting for their protracted course in some patients. We conclude that water excretion is impaired in most if not in all patients with acute infectious pneumonia (especially if extended), and that the administration of hypotonic solutions should be avoided in these patients.

Topics: Acute Disease; Aldosterone; Arginine Vasopressin; Convalescence; Diuresis; Humans; Lung; Osmolar Concentration; Pneumonia; Radiography; Renin; Sodium; Time Factors; Vasopressins; Water

Based on laboratory and clinical data from our institution, 113 patients with cirrhosis, portal hypertension, and acute hemorrhage from esophageal varices were treated with high-dose vasopressin arginine (1 to 1.5 U/min) to control the acute bleeding and reduce blood loss during portosystemic shunt operations. Compared with patients receiving a lower dose of vasopressin infusion, these patients had a reduction in both postoperative mortality (21% vs 6%) and the proportion of patients requiring emergency operation (40% vs 18%). A decrease in operative blood loss (1340 vs 793 mL) was also seen. Adverse effects of vasopressin were increased by high-dose infusion, but no significant morbidity occurred. These results suggest that high-dose vasopressin infusion can reduce the mortality of acute variceal hemorrhage and porto-systemic shunting primarily by allowing patients to improve hepatic function prior to an elective operation and by decreasing intraoperative blood loss.

Topics: Acute Disease; Adult; Aged; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Infusions, Intravenous; Male; Middle Aged; Portasystemic Shunt, Surgical; Vasopressins

Topics: Acute Disease; Adult; Aldosterone; Female; Graft Rejection; Humans; Kidney Transplantation; Male; Renin-Angiotensin System; Vasopressins

Our results reviewed here may be summarized as follows: 1. Continuous endotoxemia significantly interferes with Ca2+-dependent information flow in the liver. 2. The subcellular sites where these molecular lesions can be localized include: a.) the plasma membrane-there are effects at the level of alpha 1-adrenergic and vasopressin binding, and also in the coupling of receptor activation to inositol lipid metabolism in terms of PIP2 degradation and resynthesis b.) the endoplasmic reticulum in terms of Ca2+ release and PI synthesis. Another one of the sequelae of Ca2+-associated receptor activation, namely, cytosolic ionized Ca2+ concentration is also affected. 3. Finally, in addition to seeing the impact of acute or continuous endotoxemia at the level of receptor activation and signal generation, we can also document alterations in the expression of physiologic function subserved by these Ca2+- and inositol lipid-associated signaling processes--i.e. in glycogen phosphorylase activity-being consistent with the above described changes. In conclusion, we state that a causal link is shown between receptor binding, agonist-induced phosphoinositide hydrolysis, intracellular Ca2+ mobilization and activation of phosphorylase a in the liver, suggesting that these alterations may underlie some of the metabolic consequences of chronic sepsis.

Topics: Acute Disease; Animals; Calcium; Cell Membrane; Chronic Disease; Endotoxins; Escherichia coli; Liver; Male; Phosphatidylinositols; Phosphorylase a; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Receptors, Angiotensin; Receptors, Vasopressin; Vasopressins

We report the occurrence of acute portal vein thrombosis in three patients undergoing endoscopic variceal sclerosis (EVS) for bleeding esophageal varices. All patients received intravenous vasopressin in close proximity to or at the time of EVS. By increasing flow of sclerosant caudally into gastric veins during EVS, vasopressin may predispose to retrograde propagation of thrombus into the portal venous system. Combined use of vasopressin and EVS for treatment of bleeding esophageal varices should be undertaken with caution.

Topics: Acute Disease; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Male; Mesenteric Vascular Occlusion; Mesenteric Veins; Middle Aged; Portal Vein; Sclerosing Solutions; Thrombosis; Vasopressins

Topics: Acute Disease; Humans; Portal Vein; Sclerosing Solutions; Thrombosis; Transfusion Reaction; Vasopressins

Since bleeding from acute lesions of the gastric mucosa can cease spontaneously and the mortality rate of emergency surgery is high, conservative treatment is always preferable. Satisfactory results were obtained with continuous infusions of vasopressin in low doses (0.2 U/kg/hr for 8 hours) so that this treatment appears a valid alternative to more recent techniques (somatostatin).

Topics: Acute Disease; Adult; Aged; Female; Gastritis; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Male; Middle Aged; Peptic Ulcer Hemorrhage; Radiography; Stomach Ulcer; Vasopressins

Topics: Acute Disease; Adult; Aged; Embolization, Therapeutic; Emergencies; Female; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Male; Middle Aged; Radiography; Stomach; Vasopressins

Topics: Acute Disease; Aminopyrine; Capillary Permeability; Gastric Mucosa; Humans; Peptic Ulcer; Regional Blood Flow; Spectrophotometry; Stomach; Vasoconstriction; Vasopressins

Rats were treated with a single injection of either capsaicin (50 mg kg-1 s.c.) or vehicle on day 2 after birth. When the animals were adult, they were challenged with osmotic (water deprivation) and haemodynamic (acute hypotension) stimuli that normally evoke vasopressin release. Capsaicin-treated and vehicle-injected rats showed similar body weight losses and plasma osmolalities following 48 h of water deprivation. Thus it appears that neonatal treatment with capsaicin does not impair the antidiuretic response to plasma hyperosmolality. Following acute ganglion blockade in the presence of angiotensin converting enzyme inhibition, there was some recovery of blood pressure in the vehicle-injected rats, but recovery was significantly (P less than 0.001) less in the capsaicin-treated animals. The recovery may be attributed to vasopressin since it was abolished by an antagonist selective for the pressor action of the peptide (d(CH2)5DAVP). These results suggest that neonatal treatment with capsaicin impairs vasopressin-mediated recovery of blood pressure following acute hypotension. The possible involvement of baro- or chemoreceptor afferents is discussed.

Topics: Acute Disease; Animals; Animals, Newborn; Blood Pressure; Capsaicin; Female; Hypotension; Male; Rats; Rats, Inbred Strains; Vasopressins; Water Deprivation

A young male presented within hours after closed head injury with hypotension, tachycardia, and polyuria. A diagnosis of post-traumatic diabetes insipidus was made. Although a rare entity, the rapid diagnosis of diabetes insipidus and early treatment with vasopressin may have been life-saving in this case. A detailed approach for treatment with continuous intravenous vasopressin may be the most accurate and efficient method of managing acute onset diabetes insipidus, especially in the hemodynamically compromised patient. This will allow for a controlled fluid management in order to achieve hemodynamic stability and prevent aggravation of cerebral edema.

Topics: Acute Disease; Adult; Brain Edema; Diabetes Insipidus; Facial Bones; Humans; Male; Skull Fractures; Subarachnoid Hemorrhage; Vasopressins

As medical treatment of haemorrhage from esophageal varices vasopressin is discussed. The analogue triglycyl-vasopressin has less side-effects and a longer plasma half-life. According to the first randomized study with only a small number of patients bleeding from varices triglycyl-vasopressin was superior to vasopressin. The efficacy of somatostatin to reduce splanchnic blood flow in patients with liver cirrhosis is controversial. In a placebo-controlled trial propranolol prevented rebleeding from varices in patients with cirrhosis. However, beta-blockers should not be given to patients with advanced cirrhosis. Several controlled studies prove cimetidine not to be effective in ulcer bleeding. Somatostatin and secretin could be candidates for pharmacotherapy of haemorrhage from ulcers and erosions. In an own randomized and multicenter trial on 100 patients with stopped ulcer bleeding it was proven that the combination of the synergistically acting receptor antagonists cimetidine and pirenzepine prevent rebleeding significantly better than a prophylactic treatment of either cimetidine or pirenzepine alone. An improvement of mortality rates of upper gastrointestinal bleeding seems also to be possible by using such a combined prophylaxis. As prophylaxis of stress-ulcer bleeding cimetidine - recently ranitidine, too - and antacids are applied. Instead of a widely used enhancement of the doses of H2-blockers a combined application of H2-receptor antagonists and pirenzepine is also recommended in this indication which offers theoretical and practical advantages.

Topics: Acute Disease; Anti-Ulcer Agents; Cimetidine; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Peptic Ulcer Hemorrhage; Recurrence; Somatostatin; Vasopressins

Plasma antidiuretic hormone concentrations were measured in a group of children with acute asthma and in a control group. Very high levels of antidiuretic hormone were found in the asthmatic group. There were no changes in other biochemical indices. If overproduction of antidiuretic hormone is sustained then fluid administration to children with severe acute asthma is potentially dangerous.

Topics: Acute Disease; Asthma; Child; Child, Preschool; Female; Humans; Infant; Male; Osmolar Concentration; Sodium; Vasopressins

Topics: Acute Disease; Adenoma; Adult; Body Weight; Diabetes Insipidus; Female; Humans; Male; Middle Aged; Pituitary Neoplasms; Postoperative Complications; Solubility; Vasopressins

The use of vasopressin infusion or arterial embolization in the treatment of 87 patients with gastrointestinal hemorrhage is reviewed. A bleeding point was identified angiographically in 46 patients (53%), with a higher success rate in those with upper gastrointestinal hemorrhage (63%) than in those with lower (39%) gastrointestinal hemorrhage. Vasopressin infusion in 33 patients completely stopped hemorrhage in 14 and slowed hemorrhage pending surgery in another 5. Gelfoam embolization was successful as definitive therapy in 12 of 15 patients. Mortality as a result of hemorrhage or its sequelae was 40% in patients with upper gastrointestinal hemorrhage and 21% in those with lower gastrointestinal hemorrhage.

Topics: Acute Disease; Adolescent; Adult; Aged; Angiography; Child; Embolization, Therapeutic; Female; Gastrointestinal Hemorrhage; Gelatin Sponge, Absorbable; Humans; Infusions, Intra-Arterial; Male; Middle Aged; Vasopressins

All those who deal with patients suffering from this discouraging and lethal disease are constantly searching for the ideal method in which to control active hemorrhage from esophageal varices. Continued nonoperative management in those whose hemorrhage does cease on purely conservative measures results in an unacceptably high mortality, the most common cause of which is recurrent bleeding. Those patients who undergo portoazygos disconnection via the transabdominal or transthoracic route are equally prone to recurrent hemorrhage unless an elective portosystemic shunt is performed. Whether such a shunt is done as an elective or as an emergency procedure, the postoperative mortality and morbidity are high. Although protection against recurrent bleeding can be expected in most, the natural history of liver disease progression (and prognosis therefrom) remains unaltered, if not occasionally aggravated. Resurgence of interest in injection sclerotherapy for immediate control of hemorrhage, with subsequent longterm control of varices by repeated injections at intervals of several months, has received enthusiastic support. Preservation of existing hepatocellular function, the simplicity of the technique, especially with the fibreoptic endoscope, and its likely impact on medical care costs in this disease are attractive benefits. It is not perfect, and prospective randomized controlled trials are required to prove its superiority over other forms of treatment, but it currently appears to be the most viable alternative. We are not alone in fervently hoping that portoazygos disconnection will rarely be required and that portosystemic shunting will become a superfluous procedure, comfortably consigned to the history books.

Topics: Acute Disease; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Intubation; Male; Methods; Middle Aged; Sclerosing Solutions; Vasopressins

The role of antidiuretic hormone (ADH) in the pathogenesis of renal impaired water excretion in acute respiratory failure has not been clearly delineated. Plasma sodium concentration and plasma ADH levels (radioimmunoassay) were therefore serially measured in 13 patients with acute respiratory failure (10 with acute exacerbations of chronic lung disease and three with acute lung disease) and eight "control" patients admitted ot the intensive care unit with suspected myocardial infarction. None of the patients had systemic hemodynamic, hepatic or renal dysfunction. ADH levels were significantly elevated in patients with acute respiratory failure (15.1 +/- 5.2 pg/ml versus 5.7 +/- 1.9 pg/ml, p less than 0.05) when compared with levels in control patients. The elevated ADH levels occurred despite significantly lower plasma sodium concentration (133 +/- 1 meq/liter versus 138 +/- 2 meq/liter, p less than 0.05) compared wit control values. Moreover, markedly increased ADH values (range 1.1 to 13.0 pg/ml) were often encountered in patients with acute respiratory failure despite significant hyposmolality (263 to 275 mOsm/kg H2O). This was not observed in any control patients. These results suggest that patients with acute respiratory failure are susceptible to water retention and hyposmolality due to nonosmotic release of antidiuretic hormone.

Topics: Acute Disease; Blood Gas Analysis; Body Water; Female; Humans; Kidney; Lung Diseases, Obstructive; Male; Osmolar Concentration; Prospective Studies; Respiratory Insufficiency; Sodium; Vasopressins

Topics: Acute Disease; Albuterol; Asthma; Female; Humans; Inappropriate ADH Syndrome; Middle Aged; Vasopressins

Topics: Acute Disease; Adult; Alcoholism; Brain; Brain Diseases; Female; Humans; Magnetic Resonance Spectroscopy; Male; Middle Aged; Substance Withdrawal Syndrome; Vasopressins; Water Intoxication

A dog model was established to measure the hemodynamic changes occurring during experimental pancreatitis. The effect of treatment with Trasylol and vasopressin, beginning 60 minutes after induction of pancreatitis was assessed by their effect on the pancreatic hemodynamics. The pancreatic arterial blood flow fell by 72 per cent in the dogs with induced pancreatitis and treated only with saline solution. In contrast, the pancreatic blood flow fell by 58 per cent in the Trasylol group and 80 per cent in the vasopressin group. In addition, vasopressin had a detrimental effect on the cardiac output. Neither treatment altered the changes noted in the systemic blood pressure. Trasylol had a slight beneficial effect on experimental pancreatitis when assessed by its effect on the pancreatic hemodynamics. In contrast, vasopressin had a detrimental effect on the pancreatic hemodynamics.

Topics: Acute Disease; Animals; Aprotinin; Blood Pressure; Cardiac Output; Dogs; Hemodynamics; Pancreas; Pancreatitis; Regional Blood Flow; Vasopressins

Topics: Acute Disease; Adult; Aged; Diverticulum, Colon; Duodenal Ulcer; Gastritis; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Mallory-Weiss Syndrome; Middle Aged; Peptic Ulcer Hemorrhage; Radiography; Stomach; Stomach Ulcer; Varicose Veins; Vasopressins

Angiography is of value in the diagnosis and interventional therapy of diffuse hepatocellular disease. Hepatic arteriography is the primary diagnostic method; hepatic venography, portal venography, transvenous liver biopsy and direct cholangiography are complementary. They allow the assessment of type and stage of diseases, their hemodynamic consequences and permit the differentiation of diffuse diseases from tumorous processi. Selective vasopressin infusion and transhepatic catheter obliteration of varices are interventional techniques used to control massive bleeding from gastroesophageal varices--one of the most serious complications of diffuse hepatocellular diseases.

Topics: Acute Disease; Angiography; Budd-Chiari Syndrome; Cholangiography; Chronic Disease; Embolization, Therapeutic; Esophageal and Gastric Varices; Hepatic Veins; Hepatitis; Hepatitis, Alcoholic; Hepatitis, Viral, Human; Humans; Liver Cirrhosis; Phlebography; Portal Vein; Vasopressins

Aggressive treatment with H(2) receptor blocking agents and/or antacids has been advocated as effective prophylaxis against and treatment for "stress ulcer," based on the logical but infrequently tested assumption that the severity of the disease is critically determined by the concentration of intraluminal acid. The present study investigated this assumption in a model which employed topical acid, topical bile acid and mucosal ischemia to induce ulcerogenesis. With vascularized, chambered ex vivo wedges of canine proximal gastric wall, groups of animals were studied during three sequential periods using topical test solutions (TS) containing either 0 mM, 100 mM or 160 mM HCI. During period 1, mucosae were exposed to TS alone; during period 2, either to TS containing 1 mM sodium taurocholate (TC) or to TS and concomitant vasopressin infusion (VP); and during period 3, to TS + TC + VP. Parameters evaluated included net H(+) flux ( big up tri, openH(+)), aminopyrine clearance (AC), a measure of mucosal blood flow, net TC flux ( big up tri, openTC) and the lesion index, graded 0-5. The data indicate that in nonischemic mucosa exposed to constant [TC], AC was significantly increased, big up tri, openH(+) ("back-diffusion") increased as a linear function of [H(+)] and no lesions were observed. Under the same circumstances in ischemic mucosa, big up tri, openH(+) increased as linear function of [H(+)]. As a consequence, lesion severity was also a linear function of [H(+)]. big up tri, openTC was enhanced at low pH but bore no relation to the degree of mucosal damage induced. Assuming applicability of the model, these studies provide support for the use of H(2) receptor blocking agents and/or antacids to prevent or ameliorate "stress ulcer" disease.

Topics: Acute Disease; Administration, Topical; Aminopyrine; Animals; Bile Acids and Salts; Disease Models, Animal; Dogs; Female; Gastric Mucosa; Humans; Hydrogen-Ion Concentration; Ischemia; Male; Stomach Ulcer; Stress, Psychological; Taurocholic Acid; Vasopressins

Topics: Acute Disease; Adult; Female; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Radiography; Vasoconstrictor Agents; Vasopressins

Topics: Acute Disease; Carbamazepine; Chlorpropamide; Chronic Disease; Clofibrate; Diabetes Insipidus; Diagnosis, Differential; Humans; Saline Solution, Hypertonic; Vasopressins

Topics: Acute Disease; Animals; Blood Pressure; Blood Volume; Cardiac Output; Dogs; Hemorrhage; Liver Circulation; Portal System; Vasopressins

The hypothalamohypophyseal neurosecretory system (HHNS) was examined in the deceased from myocardial infarctions and chronic cardiac insufficiency. All 80 cases of infarctions showed in increased functional activity of the HHNS, irrespective of the time from the beginning of the disease. If the infarction was complicated by decompensation, the HHNS was characterized by hypervasopressure accompanied by occurrence of small vacuolized cells in the supraoptical nuclei with a low secretion content and high activity of biosynthetical enzymes, and a drop of secretion in the neurohypophysis. In chronic cardiac insufficiency (50 cases) there were 2 variants of changes in the HHNS, which correlated with the level of sympathetic nervous system activity (which was vitally determined from the diurnal catecholamine excretion). With high sympathetic activity, the changes in the HHNS were identical to those in myocardial infarctions, complicated by decompensation. The low activity was associated with HHNS depletion, which correlated with patients' nonsusceptibility to pathogenetic therapy.

Topics: Acute Disease; Chronic Disease; Glutamate Dehydrogenase; Heart Failure; Humans; Hypothalamo-Hypophyseal System; Myocardial Infarction; NADPH Dehydrogenase; Potassium; Sodium; Sympathetic Nervous System; Vasopressins

Short-time disturbances of the microcirculation in rabbits had a different influence on the ATP-ase activity of smooth and rough microsomes of the liver and heart. Mg+2ATP-ase activity in the liver decreased in both microsome fractions; as in the heart, the enzyme activity increased only in the smooth (light) microsomes.

Topics: Acute Disease; Adenosine Triphosphatases; Animals; Coronary Disease; Dextrans; Enzyme Activation; Glucose-6-Phosphatase; Male; Microcirculation; Microsomes; Microsomes, Liver; Myocardium; Rabbits; Time Factors; Vasopressins

Topics: Acute Disease; Animals; Blood Pressure; Dogs; Glomerular Filtration Rate; Heart Diseases; Male; Osmolar Concentration; p-Aminohippuric Acid; Pulmonary Artery; Vasopressins; Water

The authors report the case of a patient who presented, during two exacerbations of intermittent acute porphyria, a grave psychiatric syndrome secondary to severe hyponatraemia. The later was due to inappropriate secretion of anti-diuretic hormone confirmed by laboratory tests and the stimation of anti-diuretic activity in the urine. The course was favourable under the effects of symptomatic treatment including sodium supplements and fluid restriction. The anti-diuretic syndrome disappeared on each occasion without sequelae at the time of regression of the exacerbation of porphyria.

Topics: Acute Disease; Hyponatremia; Porphyrias; Recurrence; Vasopressins

Topics: Acute Disease; Arginine Vasopressin; Humans; Hyponatremia; Kidney Concentrating Ability; Vasopressins

Topics: Acute Disease; Administration, Topical; Aminopyrine; Animals; Bile Acids and Salts; Dogs; Gastric Mucosa; Hydrogen; Ischemia; Methylprednisolone; Sodium; Stomach Ulcer; Vasopressins

3 cases of inappropriate vasopressin secretion during one case of anaplastic carcinoma of the lung, one case of carcinoma of the prostate with bony metastases and one case of acute intermittent porphyria are presented. The plasma levels of vasopressin, measured by radioimmunoassay were high. Treatment with demeclocycline was attempted in one case. The clearance of free water was positive but the treatment was poorly tolerated by the digestive tract.

Topics: Acute Disease; Aged; Carcinoma; Demeclocycline; Female; Humans; Lung Neoplasms; Male; Paraneoplastic Endocrine Syndromes; Porphyrias; Prostatic Neoplasms; Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Acute Disease; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Radiography; Vasopressins

Acute hemorrhagic pancreatitis was created in dogs using the closed duodenal loop technique. After 18 hours, a a constant rate of pancreatic exocrine secretion was stimulated with secretin. A direct relationship was observed between the percentage inhibition of secretin-stimulated pancreatic exocrine flow and the dose of antidiuretic hormone administered to dogs with acute hemorrhagic pancreatitis. The acute hemorrhagic pancreatitis reduced the sensitivity of the exocrine pancreas to secretin and antidiuretic hormone.

Topics: Acute Disease; Animals; Disease Models, Animal; Dogs; Hemorrhage; Pancreas; Pancreatitis; Secretin; Vasopressins

A 72-year-old man developed the syndrome of inappropriate antidiuretic hormone secretion after sustaining an acute myocardial infarction. Other documented causes of this syndrome were excluded, and this case is therefore reported as a new association.

Topics: Acute Disease; Aged; Humans; Male; Myocardial Infarction; Osmolar Concentration; Vasopressins

Nine episodes of the syndrome of inappropriate antidiuretic hormone secretion occurred in five newborn infants following atelectasis or pneumothorax. All infants had pre-existing lung disease and were being treated with positive pressure ventilation. The mean interval between acute atelectasis or pneumothorax and the development of diagnostic hyponatremia, hypo-osmolal serum, hyperosmolal urine, and oliguria was 13.4 hours. Fluid restriction and removal of the triggering event resulted in resolution of the abnormalities within 1.5 to 4 days. Infants who develop atelectasis or pneumothorax should be evaluated for the subsequent occurrence of SIADH; the administration of a water load to them may result in dilutional hyponatremia, for which fluid restriction, not sodium infusion, is the proper therapy.

Topics: Acute Disease; Humans; Infant, Newborn; Infant, Newborn, Diseases; Osmolar Concentration; Pneumothorax; Pulmonary Atelectasis; Sodium; Syndrome; Vasopressins

In 100 patients with different forms of cerebral strokes the author studied the general water content. Its distribution in the organism. Na and K concentration in the plasma and erythrocytes and the general electrolyte content in spaces of the body. It was established that the most frequent syndromes of water-electrolyte disorders in the acute period of strokes is intracellular or general hydratation (81%). In parenchymatous-subarachnoidal hemorrhages the general dehydratation was combined with a hyperhydratation of the extracellular space, while in sichemic strokes there was an anhydridemia up to 10-18 days. A disturbance of the electrolyte metabolism was also expressed in a transmineralization with a drop of the general Na and K content due to intracellular losses. The K deficit was averagely 29% and the Na--15.5% and should be taken into consideration in a substitutive hydro-electrolyte therapy. Solutions with an increased K content should be used in order to compensate its deficit.

Topics: Acute Disease; Adrenal Cortex; Body Water; Cerebral Hemorrhage; Cerebrovascular Disorders; Extracellular Space; Humans; Hypothalamus; Mineralocorticoids; Plasma Volume; Potassium; Sodium; Time Factors; Vasopressins; Water-Electrolyte Imbalance

A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). Skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. Review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.

Topics: Acute Disease; Adult; Blood; Diabetes Insipidus; Humans; Hypothalamus; Kidney Concentrating Ability; Male; Osmolar Concentration; Polyuria; Respiratory Tract Infections; Thirst; Vasopressins

Emergency fiberoptic panendoscopy and visceral angiography both had comparable diagnostic accuracy in our series of 55 patients with actively bleeding upper gastrointestinal lesions. The diagnostic accuracy of the barium meal was found inferior to both fiberoptic panendoscopy and visceral angiography. Panendoscopy proved capable of quickly and safely diagnosing site and source of the active bleeding lesion. Visceral angiography requiring additional time, expense and personnel commitment proved an effective back-up procedure when panendoscopy was unsuccessful or contradictions existed. Emergency angiography was well tolerated by gravely ill patients. The therapeutic advantage of angiography with infusion of vasopressin upon completion of the diagnostic study remains to be shown as an advantage over panendoscopy.

Topics: Acute Disease; Adult; Angiography; Celiac Artery; Diagnostic Errors; Esophageal and Gastric Varices; Female; Fiber Optic Technology; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Male; Mesenteric Arteries; Middle Aged; Vasopressins

Topics: Acute Disease; Angiography; Gastrointestinal Hemorrhage; Humans; Vasopressins

Principles of management of bleeding esophageal varices are 1. fluid therapy of bleeding shock, 2. prevention of hepatic coma, 3. emergency endoscopy, 4. balloon tubes (Senkstaken-Blakemore, Linton-Nachlas), and 5. with some restriction, selective infusion of vasopressin into the a. mesenterica superior. If these procedures fail, sclerosing of esophageal varices stops bleeding in more than 90% of the cases. Bleeding from varices of the gastric fundus may be stopped by gastro-esophageal disconnection (Pettinari-Hassab). Both procedures have with 15% and 25% respectively, the lowest mortality. Patients for surgical shunt are carefully selected within the interval after bleeding. Shunts are the distal splenal-renal and the mesenteric-caval anastomosis with dacron prothesis (H-shunt). The shunt is the favorable therapy for prehepatic block in patients older than 14 to 16 years. The endoscopic sclerosing of esophageal varices and the gastro-esophageal disconnection are chosen in younger patients or when shunt procedures are not possible. The posthepatic block is treated successfully by conservative means. In most cases, surgical therapy is contraindicated because of poor prognosis. When conservative measures fail, in few cases emergency endoscopic sclerosing of esophageal varices or latero-lateral porto-caval anastomosis can be tried.

Topics: Acute Disease; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Plasma Substitutes; Sclerosing Solutions; Time Factors; Vasopressins

Topics: Acute Disease; Angiography; Chronic Disease; Contrast Media; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Vasopressins

Elevated plasma antidiuretic hormone (ADH) levels were noted in seven patients with status asthmaticus during the acute illness. These values returned to normal with resolution of the disease. The mechanism of this release is not completely understood but is consistent with the hypothesis that bronchospasm leads to decreased pulmonary blood flow, decreased volume return to the left atrium, and stimulation of the atrial volume receptors regulating ADH release. Planning for fluid therapy in patients with status asthmaticus should take into account a high probability of increased plasma ADH concentration during the acute illness. Water intoxication as well as hypoxia and hypercarbia should be considered as a possible cause of an altered state of consciousness associated with status asthmaticus.

Topics: Acute Disease; Adolescent; Adult; Asthma; Child; Female; Forced Expiratory Volume; Humans; Male; Middle Aged; Vasopressins

In 11 conscious normovolaemic patients with acute or chronic pancreatitis the effect of a continuous intravenous infusion of lysine-8-vasopressin, 5 IU/70 kg b.w./20 min on the portal and the hepatic venous blood flows was studied by using multiple portal catheters, oxygen saturation measurements and an indicator dilution technique with continuous infusion of 133Xe into the portal vein or its tributaries. During vasopressin infusion the total hepatic blood flow, estimated by the Bradley technique with indocyanine green dye, was reduced to 61% of the value at rest. Owing to the simultaneously occurring streamlining of the portal venous flow with incomplete mixing of indicator and blood, the portal and hepatic venous blood flows could be measured in only 3 of 9 patients. The reduction in the portal venous blood flow during vasopressin infusion was more marked than the decrease of the total hepatic flow, corresponding to a calculated increase of the hepatic arterial flow of 50%. Total splanchnic oxygen uptake and extrahepatic splanchnic oxygen uptake were unchanged during and after infusion of vasopressin. Thus, changes in splandhnic blood flow could be estimated from changes in arteriovenous oxygen differences. Also by this method a more pronounced reduction in the portal venous than of the hepatic venous blood flow was observed. The decrease during vasopressin infusion of the superior mesenteric venous flow was more marked than that of the splenic vein. The splanchnic circulatory changes may be different for other doses of vasopressin and in cirrhotic patients with higher hepatic arterial blood flow fractions.

Topics: Acute Disease; Adult; Chronic Disease; Female; Humans; Injections, Intravenous; Liver Circulation; Male; Middle Aged; Oxygen Consumption; Pancreatitis; Partial Pressure; Vasopressins

Acute hemorrhagic pancreatitis was experimentally induced in the dog by the closed-duodenal-loop technique. The disease process was modified and partially reversed by intravenous infusions of vasopressin, as indicated by some of our tests for pancreatitis as well as histologic examination of the pancreas.

Topics: Acute Disease; Amylases; Animals; Ascitic Fluid; Disease Models, Animal; Dogs; Hematocrit; Pancreas; Pancreatitis; Vasopressins

Angiography has added a new dimension to the management of hemorrhage from the large bowel. In patients with diverticular hemorrhage, mesenteric angiography not only localizes the bleeding site but, in addition, the bleeding can be acutely controlled with intraarterial infusion of vasopressin, making an emergency colectomy unnecessary. Similarly in patients bleeding from inflammatory bowel disease or in patients with post-operative hemorrhage, angiography provides information about the nature of the lesion and selective arterial infusions of vasopressin can control the bleeding. At times intestinal varices have angiographically been demonstrated as a potential source of rectal hemorrhage while in patients with unexplained lower gastrointestinal bleeding and repeatedly negative barium and endoscopic examinations, angiography has been valuable for the diagnosis of angiodysplasia of the colon.

Topics: Acute Disease; Aged; Angiography; Blood Vessels; Colitis, Ulcerative; Colon; Colonic Neoplasms; Diverticulum, Colon; Endoscopy; Gastrointestinal Hemorrhage; Humans; Intestinal Polyps; Intestine, Large; Male; Mesenteric Arteries; Middle Aged; Varicose Veins; Vasopressins

The effects of superior mesenteric arterial and intravenous infusions of vasopressin and low and high dose intravenous infusions of vasopressin on splanchnic and systemic hemodynamics were compared in 20 anesthetized dogs. The following parameters were evaluated: flow in the superior mesenteric artery and portal vein, portal and systemic blood pressure, and cardiac output. In the comparison of selective arterial and intravenous infusions, no statistically significant difference was found between the degree of changes in portal flow, portal and systemic blood pressure, and cardiac output. Only the superior mesenteric artery flow showed a greater decrease with the selective arterial injection. In a comparison of intravenous high dose (corresponding to that used clinically) and low dose (one-fifth) infusions of vasopressin, a relatively high splanchnic and low systemic effectiveness of the low dose was found. It resulted in only a 15 to 20% smaller effect on flow in the superior mesenteric artery and portal vein and portal pressure; however, about 40% lesser systemic effect on arterial blood pressure and cardiac output than the high dose. The results of this experimental work warrant exploration in clinical practice, preferably by a controlled study. If clinical success in controlling hemorrhage confirms these hemodynamic results, an intravenous. low dose infusion of vasopressin would appear to be the method of choice in the vasoconstrictive therapy of gastrointestinal bleeding from varices.

Topics: Acute Disease; Animals; Blood Pressure; Cardiac Output; Dogs; Hemodynamics; Hypertension, Portal; Infusions, Parenteral; Liver; Liver Circulation; Mesenteric Arteries; Microspheres; Portal System; Portal Vein; Vasopressins

The authors describe three postmenopausal women with agitated psychotic depression, increased water ingestion, and electrolyte values consistent with the syndrome of inappropriate antidiuretic hormone (ADH) secretion. They hypothesize that this clinical triad represents a syndrome reflecting underlying dysfunction of the hypothalamus and limbic system of the brain. The diagnosis of inappropriate ADH in one of the patients was directly confirmed by a recently developed serum radioimmunoassay.

Topics: Acute Disease; Adult; Drinking; Female; Humans; Hypothalamus; Limbic System; Middle Aged; Psychotic Disorders; Radioimmunoassay; Syndrome; Vasopressins

Topics: Acute Disease; Anuria; Child; Craniopharyngioma; Depression, Chemical; Diabetes Insipidus; Female; Humans; Injections, Intravenous; Phenytoin; Pituitary Neoplasms; Postoperative Care; Postoperative Complications; Secretory Rate; Sodium; Stimulation, Chemical; Time Factors; Vasopressins

Topics: Acute Disease; Bronchial Neoplasms; Humans; Lung Diseases; Sensory Receptor Cells; Smoking; Stress, Psychological; Vasopressins

Topics: Acute Disease; Adult; Ataxia; Barbiturates; Consciousness Disorders; Craniocerebral Trauma; Electroencephalography; Epilepsy; Female; Humans; Hyponatremia; Nystagmus, Pathologic; Porphobilinogen; Porphyrias; Urinary Incontinence; Vasopressins; Water-Electrolyte Balance

Topics: Acute Disease; Adult; Aged; Angiography; Arteries; Celiac Artery; Duodenum; Endoscopy; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Injections, Intra-Arterial; Male; Mesenteric Arteries; Middle Aged; Perfusion; Stomach; Vasopressins

Topics: Acute Disease; Duodenal Ulcer; Epinephrine; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Portography; Stomach Ulcer; Vasopressins

Topics: Acute Disease; Adult; Aged; Chronic Disease; Female; Gastrointestinal Motility; Herpes Zoster; Humans; Injections, Intramuscular; Lysine; Male; Middle Aged; Neuralgia; Osteoporosis; Pruritus; Raynaud Disease; Tabes Dorsalis; Time Factors; Trigeminal Neuralgia; Vasopressins

Topics: Acute Disease; Adrenocorticotropic Hormone; Adult; Humans; Male; Middle Aged; Phenothiazines; Pigments, Biological; Psychoses, Alcoholic; Schizophrenia; Suicide; Vasopressins

Topics: Acute Disease; Animals; Dogs; Hemorrhage; Pancreas; Pancreatitis; Prognosis; Vasopressins

Topics: Acute Disease; Age Factors; Diuresis; Female; Glomerular Filtration Rate; Humans; Hyponatremia; Middle Aged; Natriuresis; Neurologic Manifestations; Porphyrias; Vasopressins; Water-Electrolyte Balance

Topics: Acute Disease; Blood Transfusion; Emergencies; Esophageal and Gastric Varices; Esophagoscopy; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Liver Cirrhosis; Methods; Middle Aged; Vasopressins

Topics: Acute Disease; Animals; Blood Flow Velocity; Blood Pressure; Blood Proteins; Chronic Disease; Creatinine; Dogs; Glomerular Filtration Rate; Hematocrit; In Vitro Techniques; Kidney; Natriuresis; Organ Size; Oxygenators; Perfusion; Potassium; Sodium; Vasopressins

Topics: Acute Disease; Adenosine Triphosphate; Alkaloids; Animals; Arrhythmias, Cardiac; Asphyxia; Drug Synergism; Electrocardiography; Epinephrine; Fluorides; Glycogen; Hypercapnia; Male; Norepinephrine; Quinidine; Rats; Vasopressins

Topics: Acute Disease; Adult; Amino Acids; Chlorides; Extracellular Space; Female; Humans; Hypokalemia; Hyponatremia; Levulinic Acids; Male; Nitrogen; Porphobilinogen; Porphyrias; Porphyrins; Uremia; Vasopressins; Water-Electrolyte Balance

Topics: Acute Disease; Adolescent; Adult; Aged; Angiography; Arteriosclerosis; Celiac Artery; Crohn Disease; Duodenal Ulcer; Epinephrine; Esophageal and Gastric Varices; Female; Follow-Up Studies; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Injections, Intra-Arterial; Male; Mallory-Weiss Syndrome; Mesenteric Arteries; Middle Aged; Peptic Ulcer Hemorrhage; Propranolol; Vasoconstrictor Agents; Vasopressins

Topics: Acute Disease; Adolescent; Adult; Angiography; Animals; Blood Vessels; Catheterization; Celiac Artery; Child, Preschool; Dogs; Epinephrine; Gastrointestinal Hemorrhage; Hepatic Artery; Humans; Injections, Intra-Arterial; Mesenteric Arteries; Methods; Propranolol; Time Factors; Vasoconstrictor Agents; Vasopressins

1. Splenic arterial flow and splenic weight were recorded in cats anaesthetized with sodium pentobarbitone. The responses of the spleen to catecholamines, angiotensin and vasopressin were investigated.2. Catecholamines caused responses mediated by alpha- and beta-adrenoceptors in the arteriolar smooth muscle, but only insignificant beta-adrenoceptor responses could be elicited from the capsular smooth muscle. The difficulties in elucidating the mechanism of action of catecholamines on arteriolar smooth muscle are discussed.3. Angiotensin caused marked vasoconstriction, but contraction of the capsular smooth muscle was less marked. Vasopressin caused vasoconstriction but had no effect on capsular smooth muscle. Thus these peptides constrict the resistance vessels but produce much weaker contraction of the capsule.4. These responses are discussed in relation to the splenic responses to acute haemorrhage.

Topics: Acute Disease; Anesthesia, Intravenous; Angiotensin II; Animals; Catecholamines; Cats; Constriction; Hemorrhage; Injections, Intravenous; Muscle, Smooth; Organ Size; Pentobarbital; Regional Blood Flow; Spleen; Vasopressins

Topics: Acute Disease; Adult; Aged; Alcoholism; Animals; Colitis; Colitis, Ulcerative; Diverticulum, Colon; Dogs; Epinephrine; Female; Gastrointestinal Hemorrhage; Humans; Ileitis; Injections, Intra-Arterial; Male; Mesenteric Arteries; Middle Aged; Peptic Ulcer Hemorrhage; Propranolol; Regional Blood Flow; Stomach Ulcer; Vasoconstrictor Agents; Vasopressins

Topics: Acetates; Acute Disease; Adult; Chlorides; Coma; Cortisone; Craniopharyngioma; Diabetes Insipidus; Diet Therapy; Electrocardiography; Humans; Hypernatremia; Hypokalemia; Male; Natriuresis; Osmolar Concentration; Paralysis; Pituitary Neoplasms; Postoperative Complications; Potassium; Sodium; Thirst; Thyroxine; Vasopressins

Topics: Acute Disease; Humans; Hyponatremia; Infusions, Parenteral; Male; Middle Aged; Tuberculosis, Miliary; Tuberculosis, Pulmonary; Vasopressins; Water-Electrolyte Balance

Topics: Acute Disease; Adult; Humans; Hyponatremia; Male; Middle Aged; Porphyrias; Syndrome; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Acute Disease; Aldosterone; Angiotensin II; Animals; Anuria; Dogs; Glomerular Filtration Rate; Hypertension, Renal; Kidney; Liver Cirrhosis; Male; Organ Size; Renal Veins; Renin; Sodium; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Acute Disease; Adrenocorticotropic Hormone; Adult; Chronic Disease; Female; Humans; Hypothalamo-Hypophyseal System; Male; Metyrapone; Middle Aged; Multiple Sclerosis; Neurologic Manifestations; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Stimulation, Chemical; Vasopressins

Topics: Acute Disease; Animals; Gastric Mucosa; Gastritis; Gastrointestinal Hemorrhage; Rats; Vasopressins

Topics: Acute Disease; Animals; Dogs; Pancreas; Pancreatitis; Vasopressins