pituitrin and Hyperglycemia

This is a review of the management of septic shock that suggests an approach to treatment (ABCDEF: Airway, Breathing, Circulation, Drugs, Evaluate the source of sepsis, Fix the source of sepsis) for clinicians. The incidence of septic shock is increasing and mortality ranges from 30% to 70%. The commonest sources of infection are lung (25%), abdomen (25%), and other sources. Septic shock occurs because of highly complex interactions between the infecting microorganism(s) and the responses of the human host. The innate immune response is rapidly followed by the more specific adaptive immune response. Septic shock is characterized by alterations in the coagulant/anticoagulant balance such that there is a more pro-coagulant phenotype. Lung protective ventilation (which means the use of relatively low tidal volumes of 4 -6 mL/kg ideal body weight) is recommended for treatment of patients who have septic shock. Rivers early goal-directed therapy is recommended because it showed a significant increase in survival. Surviving Sepsis guidelines recommend resuscitation of septic shock with either crystalloid or colloid. Patients who have septic shock should be treated with intravenous broad-spectrum antibiotics as rapidly as possible and certainly within one hour. Activated protein C (APC) is a vitamin K dependent serine protease that is an anticoagulant and is also cytoprotective and anti-inflammatory. APC (24 mg/kg/hour infusion for 96 hours) decreased mortality (APC 25% vs placebo 31%, relative risk 0.81P=0.005) and improved organ dysfunction in patients at high risk of death (e.g. APACHE II >25 [APC 31% vs placebo 44%]). APC is not recommended to treat surgical patients who have one organ system dysfunction. In 2006, the European regulatory authority indicated that there must be another randomized placebo-controlled trial of APC to further establish efficacy as assessed by mortality reduction. Vasopressin is a key stress hormone in response to hypotension. The VASST study was a randomized trial of vasopressin versus norepinephrine in septic shock. There was no difference in mortality between vasopressin versus norepinephrine-treated patients (35% versus 39% respectively). In patients who had less severe septic shock, patients treated with vasopressin may have lowered mortality compared with norepinephrine (26% vs 36%). Annane et al. found that hydrocortisone plus fludrocortisone (compared to placebo) was associated with lower mortality in patients who had an in

Topics: Adrenal Cortex Hormones; Anemia; Anti-Bacterial Agents; Anticoagulants; Blood Coagulation; Fluid Therapy; Humans; Hyperglycemia; Hypoglycemic Agents; Insulin; Protein C; Renal Insufficiency; Shock, Septic; Vasopressins

Topics: Adrenal Cortex Hormones; Anemia; Anti-Bacterial Agents; Blood Coagulation Factors; Humans; Hyperglycemia; Hypoglycemic Agents; Immune Tolerance; Insulin; Protein C; Renal Replacement Therapy; Respiration, Artificial; Sepsis; Vasopressins

Cushing's syndrome is a consequence of primary or, more commonly, secondary oversecretion of cortisol. Cardiovascular disease is the major cause of morbidity and mortality in Cushing's syndrome, and excess risk remains even in effectively treated patients. The cardiovascular consequences of cortisol excess are protean and include, inter alia, elevation of blood pressure, truncal obesity, hyperinsulinemia, hyperglycemia, insulin resistance, and dyslipidemia. This review analyses the relationship of cortisol excess, both locally and at tissue level, to these cardiovascular risk factors, and to putative mechanisms for hypertension. Previous studies have examined correlations between cortisol, blood pressure, and other parameters in the general population and in Cushing's syndrome. This review also details changes induced by short-term cortisol administration in normotensive healthy men.

Topics: Blood Pressure; Cardiac Output; Cardiovascular Diseases; Cushing Syndrome; Female; Humans; Hydrocortisone; Hyperglycemia; Hyperlipidemias; Hypertension; Insulin Resistance; Male; Obesity; Plasma Volume; Renin-Angiotensin System; Risk Factors; Sympathetic Nervous System; Vascular Resistance; Vasodilation; Vasopressins

Topics: Anesthetics; Animals; Brain; Brain Stem; Cerebral Ventricles; Epinephrine; History, 20th Century; Humans; Hyperglycemia; Morphine; Neurochemistry; Sympatholytics; Vasopressins

Topics: Adrenal Cortex Hormones; Arrhythmias, Cardiac; Cardiovascular Diseases; Catecholamines; Cerebrovascular Disorders; Humans; Hyperglycemia; Hypertension; Hyponatremia; Models, Biological; Pulmonary Edema; Vasopressins

Topics: Adult; Animals; Body Fluid Compartments; Body Fluids; Body Water; Brain; Dehydration; Diabetes Insipidus; Extracellular Space; Glucose; Homeostasis; Humans; Hyperglycemia; Infant, Newborn; Intracellular Fluid; Male; Osmolar Concentration; Plasma; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Analgesics, Opioid; Animals; Blood Pressure; Brain Stem; Humans; Hyperglycemia; Neurons; Subarachnoid Space; Vasopressins

Previous trials have suggested that vasopressin and methylprednisolone administered during in-hospital cardiac arrest might improve outcomes.. To determine whether the combination of vasopressin and methylprednisolone administered during in-hospital cardiac arrest improves return of spontaneous circulation.. Multicenter, randomized, double-blind, placebo-controlled trial conducted at 10 hospitals in Denmark. A total of 512 adult patients with in-hospital cardiac arrest were included between October 15, 2018, and January 21, 2021. The last 90-day follow-up was on April 21, 2021.. Patients were randomized to receive a combination of vasopressin and methylprednisolone (n = 245) or placebo (n = 267). The first dose of vasopressin (20 IU) and methylprednisolone (40 mg), or corresponding placebo, was administered after the first dose of epinephrine. Additional doses of vasopressin or corresponding placebo were administered after each additional dose of epinephrine for a maximum of 4 doses.. The primary outcome was return of spontaneous circulation. Secondary outcomes included survival and favorable neurologic outcome at 30 days (Cerebral Performance Category score of 1 or 2).. Among 512 patients who were randomized, 501 met all inclusion and no exclusion criteria and were included in the analysis (mean [SD] age, 71 [13] years; 322 men [64%]). One hundred of 237 patients (42%) in the vasopressin and methylprednisolone group and 86 of 264 patients (33%) in the placebo group achieved return of spontaneous circulation (risk ratio, 1.30 [95% CI, 1.03-1.63]; risk difference, 9.6% [95% CI, 1.1%-18.0%]; P = .03). At 30 days, 23 patients (9.7%) in the intervention group and 31 patients (12%) in the placebo group were alive (risk ratio, 0.83 [95% CI, 0.50-1.37]; risk difference: -2.0% [95% CI, -7.5% to 3.5%]; P = .48). A favorable neurologic outcome was observed in 18 patients (7.6%) in the intervention group and 20 patients (7.6%) in the placebo group at 30 days (risk ratio, 1.00 [95% CI, 0.55-1.83]; risk difference, 0.0% [95% CI, -4.7% to 4.9%]; P > .99). In patients with return of spontaneous circulation, hyperglycemia occurred in 77 (77%) in the intervention group and 63 (73%) in the placebo group. Hypernatremia occurred in 28 (28%) and 27 (31%), in the intervention and placebo groups, respectively.. Among patients with in-hospital cardiac arrest, administration of vasopressin and methylprednisolone, compared with placebo, significantly increased the likelihood of return of spontaneous circulation. However, there is uncertainty whether this treatment results in benefit or harm for long-term survival.. ClinicalTrials.gov Identifier: NCT03640949.

Topics: Aged; Cardiovascular Agents; Confidence Intervals; Denmark; Double-Blind Method; Epinephrine; Female; Glucocorticoids; Heart Arrest; Humans; Hyperglycemia; Hyponatremia; Male; Methylprednisolone; Neurologic Examination; Placebos; Return of Spontaneous Circulation; Treatment Outcome; Uncertainty; Vasoconstrictor Agents; Vasopressins

Surgery causes changes in hemostasis, leading to a hypercoagulable state that has been linked to both arterial and venous thrombotic complications. The etiology of this state is unknown, but many investigators have hypothesized that perioperative neuroendocrine changes are responsible. We have previously demonstrated minimal increases in hemostatic function with a stress hormone infusion. This study was undertaken to further examine the relationship between neuroendocrine hormones and hemostatic function. Seventeen healthy volunteers were administered a stress hormone cocktail i.v. (epinephrine, cortisol, glucagon, angiotensin II, and vasopressin) for 24 h in a blind, placebo-controlled, cross-over design in our clinical research center. Venous blood samples were obtained for measurement of hemostatic function before the infusion and at 2, 8, and 24 h. There were no demonstrable increases in any measure of hypercoagulability. Alternatively, there was an increase in tissue plasminogen activator and protein C activity. These changes are consistent with an inhibition of coagulation and improved fibrinolysis. These data suggest that this combination of neuroendocrine hormones is not responsible for the postoperative hypercoagulable state.. Infusion of five stress hormones (epinephrine, cortisol, glucagon, vasopressin, and angiotensin II) to normal volunteers does not cause increases in procoagulant proteins and platelet reactivity or decreases in fibrinolytic proteins. Alternatively, these five hormones caused increased levels of fibrinolytic proteins (tissue plasminogen activator) and endogenous anticoagulants (protein C antigen and activity).

Topics: Adult; Angiotensin II; Blood Coagulation; Epinephrine; Female; Glucagon; Hemodynamics; Humans; Hydrocortisone; Hyperglycemia; Leukocyte Count; Male; Norepinephrine; Plasminogen Activator Inhibitor 1; Platelet Count; Postoperative Period; Protein C; Stress, Physiological; Time Factors; Tissue Plasminogen Activator; Vasopressins

Short sleep is linked to disturbances in glucose metabolism and may induce a prediabetic condition. The biological clock in the suprachiasmatic nucleus (SCN) regulates the glucose rhythm in the circulation and the sleep-wake cycle. SCN vasopressin neurons (SCN

Topics: Animals; Circadian Rhythm; Diabetes Mellitus, Type 2; Glucose; Glucose Transporter Type 1; Hyperglycemia; Rats; Sleep; Suprachiasmatic Nucleus; Vasopressins

In the last decade, cross-sectional and multiple cohort studies have associated total fluid intake or water intake with the risk for chronic kidney disease (CKD) and even the risk of developing hyperglycemia. Urine biomarkers have also been linked to the risk of CKD and lithiasis, and these biomarkers respond quickly to variations in fluid intake. High circulating copeptin levels, a surrogate marker of arginine vasopressin, have been associated with metabolic syndrome, renal dysfunction and increased risk for diabetes mellitus, cardiovascular disease and death. The aim of this paper was to explore how the various findings on water intake, hydration and health are interconnected, to highlight current gaps in our understanding and to propose a model that links water intake, homeostatic mechanisms to maintain water balance and health outcomes. Since plasma copeptin and vasopressin have been demonstrated to be sensitive to changes in water intake, inversely associated with 24-hour urine volume, and associated with urine biomarkers and fluid intake, vasopressin is proposed as the central player in this theoretical physiological model.

Topics: Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Diabetes Mellitus; Drinking; Glycopeptides; Health Status; Humans; Hyperglycemia; Metabolic Syndrome; Models, Biological; Renal Insufficiency, Chronic; Risk Factors; Vasopressins; Water-Electrolyte Balance

Reliable data at population level are essential to firmly establish links between fluid intake, hydration and health, investigate dose-response relationships and develop meaningful public health strategies or reference intake values. However, limited research exists regarding the most appropriate methodology for assessing beverage or total fluid intake (TFI). To date, methodologies have been developed to assess food and nutrient intake without due consideration of water or fluid intake behavior. A recent crossover study showed that a 24-hour food recall significantly underestimated mean TFI by 382 ml (95% CI 299-465) compared with a fluid specific 7-day record. The authors postulated that this average difference was mainly the result of missed drinking acts between meals a 24-hour recall was used. Using a 7-day record administered in paper form or on-line has also been shown to lead to a significantly different mean TFI of 129 ml. Therefore, the choice of methodology might result in measurement errors that limit between-survey or between-country comparisons. Such errors may contribute to variations in estimates of TFI that cannot be explained by differences in climate, physical activity or cultural habits. A recent survey confirmed the variation in methodologies used in European national dietary surveys. Since these surveys form the basis for setting adequate intakes for total water intake, measurement error between surveys should be limited, highlighting the need for the development of a consistent methodology that is validated for water and TFI estimation.

Topics: Arginine Vasopressin; Biomarkers; Cardiovascular Diseases; Dehydration; Drinking; Female; Glomerular Filtration Rate; Glycopeptides; Health Status; Humans; Hyperglycemia; Male; Metabolic Syndrome; Models, Biological; Prognosis; Renal Insufficiency, Chronic; Risk Factors; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Accidents, Traffic; Adult; Brain Edema; Brain Injuries; Catecholamines; Fatal Outcome; Glasgow Coma Scale; Hematoma, Subdural; Humans; Hyperglycemia; Hyperkalemia; Hypokalemia; Hypothermia; Insulin; Intracranial Hypertension; Male; Mannitol; Norepinephrine; Potassium; Vasopressins

Hypoxic stimulation of the carotid body receptors (CBR) results in a rapid hyperglycemia with an increase in brain glucose retention. Previous work indicates that neurohypophysectomy inhibits this hyperglycemic response. Here, we show that systemic arginine vasopressin (AVP) induced a transient, but significant, increase in blood glucose levels and increased brain glucose retention, a response similar to that observed after CBR stimulation. Comparable results were obtained after intracerebral infusion of AVP. Systemic AVP-induced changes were maintained in hypophysectomized rats but were not observed after adrenalectomy. Glycemic changes after CBR stimulation were inhibited by pharmacological blockage of AVP V1a receptors with a V1a-selective receptor antagonist ([beta-Mercapto-beta,beta-cyclopentamethylenepropionyl1,O-me-Tyr2, Arg8]-vasopressin). Importantly, local application of micro-doses of this antagonist to the liver was sufficient to abolish the hyperglycemic response after CBR stimulation. These results suggest that AVP is a mediator of the hyperglycemic reflex and cerebral glucose retention following CBR stimulation. We propose that hepatic activation of AVP V1a receptors is essential for this hyperglycemic response.

Topics: Adrenal Glands; Adrenalectomy; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Brain Chemistry; Carotid Body; Catecholamines; Chemoreceptor Cells; Enzyme Inhibitors; Glucagon; Glucose; Hyperglycemia; Hypoxia; Liver; Male; Rats; Rats, Wistar; Receptors, Vasopressin; Sodium Cyanide; Vasopressins

Daily peak plasma glucose concentrations are attained shortly before awakening. Previous experiments indicated an important role for the biological clock, located in the suprachiasmatic nuclei (SCN), in the genesis of this anticipatory rise in plasma glucose concentrations by controlling hepatic glucose production. Here, we show that stimulation of NMDA receptors, or blockade of GABA receptors in the paraventricular nucleus of the hypothalamus (PVN) of conscious rats, caused a pronounced increase in plasma glucose concentrations. The local administration of TTX in brain areas afferent to the PVN revealed that an important part of the inhibitory inputs to the PVN was derived from the SCN. Using a transneuronal viral-tracing technique, we showed that the SCN is connected to the liver via both branches of the autonomic nervous system (ANS). The combination of a blockade of GABA receptors in the PVN with selective removal of either the sympathetic or parasympathetic branch of the hepatic ANS innervation showed that hyperglycemia produced by PVN stimulation was primarily attributable to an activation of the sympathetic input to the liver. We propose that the daily rise in plasma glucose concentrations is caused by an SCN-mediated withdrawal of GABAergic inputs to sympathetic preautonomic neurons in the PVN, resulting in an increased hepatic glucose production. The remarkable resemblance of the presently proposed control mechanism to that described previously for the control of daily melatonin rhythm suggests that the GABAergic control of sympathetic preautonomic neurons in the PVN is an important pathway for the SCN to control peripheral physiology.

Topics: Animals; Axonal Transport; Bicuculline; Blood Glucose; Circadian Rhythm; Clonidine; Corticosterone; gamma-Aminobutyric Acid; Glucagon; Gluconeogenesis; Herpesvirus 1, Suid; Hyperglycemia; Hypothalamus; Insulin; Isoproterenol; Liver; Male; Microdialysis; Muscimol; N-Methylaspartate; Norepinephrine; Parasympathectomy; Parasympathetic Nervous System; Paraventricular Hypothalamic Nucleus; Rats; Rats, Wistar; Suprachiasmatic Nucleus; Sympathectomy; Sympathetic Nervous System; Tetrodotoxin; Vasopressins

Although secondary end-organ damage in diabetes has generally been thought to result from long-term passive shunting of excess glucose through alternative metabolic pathways, recent studies have elucidated a second mechanism of pathogenesis that involves active changes in gene expression in neurons of the CNS. These changes in gene expression result in molecular and functional changes that can become maladaptive over time. In this review, we examine two neuronal populations in the brain that have been studied in human beings and animal models of diabetes. First, we discuss overactivation of magnocellular neurosecretory cells within the hypothalamus and how it relates to the development of diabetic nephropathy. And second, we describe how changes in hippocampal synaptic plasticity can lead to cognitive and behavioural deficits in chronic diabetes. Changes in neuronal gene expression in diabetes represent a new pathway for diabetic pathogenesis. This pathway may hold clues for the development of therapies that, via the targeting of neurons, can slow or prevent the development of diabetic end-organ damage.

Topics: Animals; Cognition Disorders; Diabetes Mellitus; Diabetic Nephropathies; Gene Expression; Hippocampus; Humans; Hyperglycemia; Hypothalamus; Neuronal Plasticity; Neurons; Vasopressins

We studied osmoregulation of plasma vasopressin in 5 patients with newly diagnosed diabetes mellitus. All patients showed typical symptoms of uncontrolled diabetes mellitus such as marked hyperglycemia, polyuria, and polydipsia, but did not have advanced diabetic complications. Vasopressin release was studied using 5% hypertonic saline infusion test twice: before treatment when the patient was hyperglycemic, and after treatment 1 to 2 months later when the patient was euglycemic. Plasma vasopressin was measured by a sensitive and specific radioimmunoassay. The mean basal plasma vasopressin value in the patients was significantly higher in the hyperglycemic compared with the euglycemic state (3.75 +/- 0.70 vs 1.18 +/- 0.46 pmol/l, respectively; P < 0.05). The relationship of plasma vasopressin with serum sodium, but not plasma osmolality, during hyperglycemia showed an apparent hypersecretion of vasopressin. In both cases, the sensitivity of the vasopressin response to osmotic stimuli was significantly decreased. During euglycemia, the sensitivity of vasopressin secretion to either sodium or osmolality was almost normal, although a slight rise in the osmostat was observed compared with normal subjects. Together, we found that the positive correlation of vasopressin with sodium or osmolality is maintained but significantly altered in patients with untreated diabetes mellitus. Especially noteworthy is the lowered threshold and decreased sensitivity of osmotically-induced vasopressin secretion during hyperglycemia, which may be caused by multiple factors such as diabetes-associated hypovolemia, osmogenic effects of glucose and other osmoles, depletion of the pool of vasopressin available for release, and the metabolic derangement of osmoreceptor/magnocellular neurons.

Topics: Adult; Blood Glucose; Diabetes Mellitus; Female; Humans; Hyperglycemia; Hypertonic Solutions; Male; Middle Aged; Sodium; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Vasopressin (VP) is a peptide consisting of 9 amino acids which acts as a neurotransmitter or neuromodulator in the central nervous system. Neurons containing VP project to some nuclei in the hypothalamus that have a role in energy metabolism. To clarify the possible role of VP on glucose metabolism in the brain, we examined the effect of intracranial injection of VP on the hyperglycemia induced by 2-deoxy-D-glucose (2DG) and obtained the following results. The hyperglycemic and hyperglucagonemic responses induced by 2DG were significantly suppressed and enhanced by co-injections of VP and a VP-antagonist with 2DG, respectively. However, co-injections of either VP or a VP-antagonist with 2DG had no effect on the change in plasma insulin concentration. These findings suggest that central VP plays a suppressive role in the hyperglycemic and hyperglucagonemic responses to 2DG.

Topics: Animals; Blood Glucose; Deoxyglucose; Glucagon; Hyperglycemia; Hypothalamus; Insulin; Male; Rats; Rats, Wistar; Time Factors; Vasopressins

Evidence that an increase in plasma atrial natriuretic peptide (ANP) concentrations mediates, at least in part, glomerular hyperfiltration in diabetic rats prompted us to study the relationship between ANP and renal haemodynamics in hyperfiltering type 2 diabetic patients in association with other hormones implicated in the control of glomerular filtration rate (GFR) (catecholamines, vasopressin, renin) and in sodium tubular transport (aldosterone, ouabain-displacing factor, ODF). Since hyperglycaemia is also associated to hyperfiltration, diabetic patients who presented with secondary drug failure were studied both in hyperglycaemic and in normoglycaemic condition. For this purpose, 11 normotensive non-macroproteinuric hyperfiltering patients with type 2 diabetes were treated with an 8-day continuous insulin infusion (days 0-7). Dehydration was prevented or corrected and natriuresis was on day 0 above 100 mmol/day. The following parameters were determined on days 0 and 7: GFR and renal plasma flow (RPF) by 99mTc-DTPA and 131I-hippuran clearances; the extracellular volume, assimilated to the DTPA diffusion volume; urinary ODF by receptor-binding assay and urinary as well as plasma catecholamines by HPLC after extraction on alumin. Plasma ANP and antidiuretic hormone (ADH) were measured by radioimmunoassay after extraction on phenyl-silylsilica (ANP) and with ether (ADH). Unextracted plasma was used for radioimmunological measurement of plasma renin activity and aldosterone. When correcting hyperglycaemia to normoglycaemia GFR decreased from high to normal mean value (138 +/- 27 and 115 +/- 6 ml/min, p < 0.001), RPF followed the same trend, and the DTPA diffusion volume did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Atrial Natriuretic Factor; Diabetes Mellitus, Type 2; Female; Glomerular Filtration Rate; Hormones; Humans; Hyperglycemia; Insulin; Male; Middle Aged; Renal Circulation; Vasopressins

Patients with diabetes mellitus have higher levels of coagulation factor VIII than the non-diabetic population. This may be a result of poor metabolic control and could contribute to the development of microvascular complications. During ketoacidosis there are acute changes in plasma concentrations of coagulation factors, some of which may be mediated by the rise in vasopressin that occurs. We have investigated the effects of hyperglycaemia without ketosis on some aspects of haemostasis by manipulating blood glucose concentrations using a Biostator. After a 1h run-in period with the blood glucose at 5 mmol/l, the blood glucose was maintained at 5, 15 and 25 mmol/l and maintained for one hour at each level in six male patients with insulin-dependent diabetes. Insulin was infused at 0.25 mu/kg/min. Venous blood samples were taken at the beginning and end of each hour after the run-in period for assays of factor VIII coagulant activity (FVIII:C), von Willebrand factor antigen (vWF:Ag), ristocetin co-factor (FVIIIR:Co), activated partial thromboplastin time (APTT) and vasopressin (aVP). There was a slight, though statistically insignificant fall in median factor VIII:C concentration at each incremental level of increase in blood glucose. Values (at the beginning and end of each hour) were: 1.0 and 1.1 iu/ml at 5 mmol/l; 0.95 and 0.79 iu/ml at 15 mmol/l; and 0.74 and 0.84 iu/ml at 25 mmol. vWF:Ag and FVIIIR:Co were unchanged. Plasma aVP fell slightly from 1.1 to 0.5 pg/ml. The results indicate that high levels of FVIII seen in diabetes are not due to short-term increases in blood glucose and that acute hyperglycaemia does not promote pro-coagulant changes in blood.

Topics: Adolescent; Adult; Diabetes Mellitus, Type 1; Factor VIII; Humans; Hyperglycemia; Male; Partial Thromboplastin Time; Vasopressins

Hyperosmolar diabetic coma is characterised by extreme hyperglycaemia and dehydration. Hypernatremia often contributes additionally to plasma hyperosmolarity. The pathogenesis of these component abnormalities is considered. The explanation of the absence of hyperketonaemia is examined in the light of recent experimental and clinical data. At the beginning of the development of the syndrome, high peripheral plasma insulin probably explains the lack of ketosis via inhibition of lipolysis. Later, when hyperosmolar coma is established, peripheral insulinopenia but an "insulinised" liver may coexist. This would favour metabolism of free fatty acids along nonketogenic pathways.

Topics: Blood; Dehydration; Diabetic Coma; Glucagon; Humans; Hyperglycemia; Hyperglycemic Hyperosmolar Nonketotic Coma; Insulin; Kinetics; Osmolar Concentration; Sodium; Uremia; Vasopressins

Topics: Blood Volume; Diuretics; Heart Failure; Hospitalization; Humans; Hyperglycemia; Hyponatremia; Kidney Failure, Chronic; Liver Cirrhosis; Stress, Physiological; Surgical Procedures, Operative; Vasopressins

An experiment was performed in female rats in order to assess the influence and mechanism underlying the effects of hyperglycemia, hypertonic saline and vasopressin upon the gastric acid secretion and mucosal blood flow (MBF). Infusion of isotonic saline did not alter acid output and gastric clearance of plasma aminopyrine whereas hypertonic solutions (20% glucose or 3% NaCl) significantly increased plasma osmolality and decreased the acid secretion within 30 min and recovered to normal levels after 2 h. Vasopressin also effectively inhibited acid secretion. Both hypertonic solutions and vasopressin decreased the mucosal blood flow. However, the ratio (R) of MBF to gastric secretory rate which is a helpful guide to the mechanism of secretory inhibition did not significantly change in either case. We concluded that all three agents probably had a direct action on secretion rather than decreasing MBF. The mechanism of inhabition of acid secretion and its relationship to MBF was suggested and discussed.

Topics: Animals; Female; Gastric Juice; Gastric Mucosa; Glucose Solution, Hypertonic; Hyperglycemia; Hypertonic Solutions; Rats; Regional Blood Flow; Saline Solution, Hypertonic; Vasopressins

Metabolic effects of vasopressin, glucagan and adrenalin were compared, in intact rats, especially in regard to time courses of effects. Hyperglycaemia was transient in response to vasopressin, prolonged following adrenalin, and, suprisingly, was not discernible after glucagon, except in response to a very large dose. Vasopressin decreased and adrenalin increased, the plasma free fatty acid concentration; both hormones decreased the triacylglycerol level. Muscle glycogen concentrations, measured in heart, diaphragm and skeletal muscle, exhibited small changes, with complex time courses, following hormone administration. Vasopressin brought about a rapid but transient activation of heaptic glycogen phosphorylase which resembled that due to adrenalin. The activation by glucagon of phosphorylase was greater and more prolonged, despite the absence of hyperglycaemia. In response to vasopressin, there was in increase in plasma insulin. Incorporation of 14C from [14C]glucose into glycogen or fatty acids was not influenced by vasopressin. Taken together, these results may be explained by rapid metabolic action of vasopressin on hepatic glycogenolysis, whereas adrenalin has multiple prolonged actions.

Topics: Adipose Tissue; Animals; Blood Glucose; Epinephrine; Fatty Acids; Female; Glucagon; Glycogen; Hyperglycemia; Insulin; Liver; Male; Muscles; Phosphorylases; Rats; Vasopressins

Topics: Adrenal Insufficiency; Humans; Hyperglycemia; Hyperlipidemias; Hyponatremia; Pituitary Gland, Posterior; Syndrome; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Adipose Tissue; Animals; Blood Glucose; Carbon Dioxide; Carbon Isotopes; Cricetinae; Diabetes Mellitus; Dogs; Female; Glucose; Hyperglycemia; Insulin; Male; Oxytocin; Pancreatectomy; Peptides; Pituitary Hormones, Posterior; Rats; Structure-Activity Relationship; Vasopressins; Vasotocin

Topics: Animals; Dogs; Glucose; Hyperglycemia; Hypoglycemia; Insulin; Lipid Metabolism; Metabolism; Oxytocin; Peptides; Rabbits; Vasopressins

Topics: Adult; Blood Glucose; Dehydration; Diabetes Mellitus; Diabetic Coma; Diabetic Ketoacidosis; Diabetic Retinopathy; Glucose; Humans; Hyperglycemia; Hypothalamo-Hypophyseal System; Iatrogenic Disease; Insulin; Male; Pituitary Hormones, Anterior; Stress, Physiological; Vasopressins

The effects upon islet hormone secretion of highly purified preparations of secretin and of pancreozymin-cholecystokinin and of a crude gastrin-containing extract of hog antrum have been studied in acutely operated dogs. All three preparations were shown to cause a striking increase in insulin concentration in the pancreaticoduodenal venous plasma after their rapid endoportal injection in anesthetized dogs. With each hormone preparation, the peak in insulin secretion occurred 1 minute after injection, and a rapid decline was observed immediately thereafter. Whereas secretin and gastrin failed to alter significantly the pancreaticoduodenal venous glucagon or arterial glucose concentration, pancreozymin caused a dramatic rise in pancreaticoduodenal venous glucagon concentration, which reached a peak 3 minutes after injection, and hyperglycemia was noted to occur soon thereafter. Endoportal infusion of secretin and pancreozymin for 20 minutes caused responses that were sustained but qualitatively identical to the responses noted after rapid injection of the hormones. The beta-cytotropic effect of secretin was abolished by the infusion of epinephrine. These results could not be attributed to the small degree of contamination of the enteric hormone preparations with insulin or glucagon, and it would appear that secretin, pancreozymin, and probably gastrin have insulin-releasing activity and that pancreozymin has, in addition, glucagon-releasing activity.The demonstration that these three hormones possess insulin-releasing activity suggests that there is in the gastrointestinal tract a chain of betacytotropic hormones from antrum to ileum that is capable of augmenting insulin secretion as required for disposal of substrate loads. It is suggested that the existence of this "entero-insular axis" prevents high substrate concentrations that would otherwise follow ingestion of large meals were the insular response entirely a function of arterial substrate concentration.

Topics: Adrenocorticotropic Hormone; Animals; Blood Glucose; Cholecystokinin; Dogs; Epinephrine; Gastrins; Glucagon; Growth Hormone; Hyperglycemia; Insulin; Secretin; Vasopressins

Topics: Blood Chemical Analysis; Carbon Dioxide; Chlorides; Diabetes Insipidus; Diabetes Mellitus; Glucose Tolerance Test; Glycosuria; Hematuria; Humans; Hydronephrosis; Hyperglycemia; Nitrogen; Polyuria; Potassium; Pseudomonas Infections; Sodium; Urea; Urinary Tract Infections; Urine; Urography; Vasopressins

Topics: Addison Disease; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diuresis; Diuretics; Humans; Hyperglycemia; Kidney Tubules; Osmosis; Physiology; Polyuria; Syndrome; Vasopressins

Topics: Arginine Vasopressin; Humans; Hyperglycemia; Oxytocics; Oxytocin; Vasopressins