pituitrin and Myocardial-Infarction

The neurons secreting oxytocin (OXY) and vasopressin (AVP) are located mainly in the supraoptic, paraventricular, and suprachiasmatic nucleus of the brain. Oxytocinergic and vasopressinergic projections reach several regions of the brain and the spinal cord. Both peptides are released from axons, soma, and dendrites and modulate the excitability of other neuroregulatory pathways. The synthesis and action of OXY and AVP in the peripheral organs (eye, heart, gastrointestinal system) is being investigated. The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. Vasopressin interacts with three subtypes of receptors: V1aR, V1bR, and V2R whereas oxytocin activates its own OXTR and V1aR receptors. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors. The inappropriate regulation of oxytocin and vasopressin secretion during ischemia, hypoxia/hypercapnia, inflammation, pain, and stress may play a significant role in the pathogenesis of cardiovascular diseases.

Topics: Axons; Brain; Cardiovascular Abnormalities; Cardiovascular System; Humans; Hypertension; Lung; Myocardial Infarction; Neurons; Neurophysins; Oxytocin; Protein Precursors; Receptors, Oxytocin; Vasopressins

Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the major enzymes responsible for alcohol metabolism in humans. Emerging evidences have shown that functional polymorphisms in ADH and ALDH genes might play a critical role in increasing coronary artery disease (CAD) and myocardial infarction (MI) risks; however, individually published studies showed inconclusive results. The aim of this meta-analysis is to evaluate the associations between the genetic polymorphisms of ADH and ALDH genes with susceptibility to CAD and MI. A literature search was conducted on PubMed, Embase, Web of Science and Chinese BioMedical databases from inception through December 1st, 2012. Crude relative risks (RRs) with 95% confidence intervals (CIs) were calculated. Twelve case-control studies were included with a total of 9616 subjects, including 2053 CAD patients, 1436 MI patients, and 6127 healthy controls. Meta-analysis showed that mutant genotypes (GA+AA) of the rs671 polymorphism in the ALDH2 gene were associated with increased risk of both CAD and MI (CAD: RR=1.20, 95%CI: 1.03-1.40, P=0.021; MI: RR=1.32, 95%CI: 1.11-1.57, P=0.002). However, there were no significant associations of ADH genetic polymorphisms to CAD and MI risks (CAD: RR=0.92, 95%CI: 0.73-1.15, P=0.445; MI: RR=0.93, 95%CI: 0.84-1.03, P=0.148). In conclusion, this meta-analysis provides strong evidence that ALDH2 rs671 polymorphism may be associated with increased risks of CAD and MI. However, further studies are still needed to accurately determine whether ADH genetic polymorphisms are associated with susceptibility to CAD and MI.

Topics: Aldehyde Dehydrogenase; Aldehyde Dehydrogenase, Mitochondrial; Coronary Artery Disease; Genetic Predisposition to Disease; Humans; Myocardial Infarction; Neurophysins; Polymorphism, Genetic; Protein Precursors; Publication Bias; Risk; Vasopressins

Arginine vasopressin (AVP or antidiuretic hormone) is one of the key hormones in the human body responsible for a variety of cardiovascular and renal functions. It has so far escaped introduction into the routine clinical laboratory due to technical difficulties and preanalytical errors. Copeptin, the C-terminal part of the AVP precursor peptide, was found to be a stable and sensitive surrogate marker for AVP release. Copeptin behaves in a similar manner to mature AVP in the circulation, with respect to osmotic stimuli and hypotension. During the past years, copeptin measurement has been shown to be of interest in a variety of clinical indications, including cardiovascular diseases such as heart failure, myocardial infarction, and stroke. This review summarizes the recent progress on the diagnostic use of copeptin in cardiovascular and renal diseases and discusses the potential use of copeptin measurement in the context of therapeutic interventions with vasopressin receptor antagonists.

Topics: Arginine Vasopressin; Biomarkers; Blood Volume; Cardiovascular Diseases; Cardiovascular System; Glycopeptides; Heart Failure; Humans; Kidney; Kidney Diseases; Myocardial Infarction; Prognosis; ROC Curve; Shock, Cardiogenic; Stroke; Vasopressins

Cardiogenic shock after acute myocardial infarction continues to exhibit a high mortality rate. The prognosis can be improved with acute revascularization. Use of the intra-aortic balloon pump is also an established treatment concept. Administration of catecholamines should be limited as far as possible; monitoring hemodynamic parameters based on cardiac power output or cardiac power index can be very helpful. New treatment approaches such as the calcium sensitizer levosimendan, NO synthase inhibition, complement inhibition, or vasopressin therapy have not yet yielded convincing results. Future therapies will likely address the anti-inflammatory aspect of cardiogenic shock.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Cardiotonic Agents; Catecholamines; Complement C5; Complement Inactivating Agents; Humans; Hydrazones; Intra-Aortic Balloon Pumping; Myocardial Infarction; Myocardial Revascularization; Nitric Oxide Synthase; Pyridazines; Randomized Controlled Trials as Topic; Shock, Cardiogenic; Simendan; Survival Rate; Vasopressins

Epinephrine given during cardiopulmonary resuscitation (CPR) may cause beta-mimetic complications in the postresuscitation phase. Vasopressin may be an alternative vasopressor drug during CPR. A subgroup analysis of a large prospective CPR investigation and of retrospective CPR studies suggests that vasopressin may be especially beneficial when combined with epinephrine. Beneficial effects of adding vasopressin were observed in other catecholamine-refractory shock states as well, such as vasodilatory shock and haemorrhagic shock. In order to maximize effects of any vasopressor during CPR, rapid aggressive chest compressions must be ensured to maximize blood flow and to enable advanced cardiac life support drugs to reach the arterial vasculature. We suggest alternating injections of 1 mg epinephrine i.v. and 40 IU vasopressin i.v. every 3-5 minutes during CPR until spontaneous circulation can be achieved or CPR efforts are terminated.

Topics: Cardiopulmonary Resuscitation; Drug Therapy, Combination; Epinephrine; Forecasting; Humans; Myocardial Infarction; Vasopressins

Cardiovascular failure in critically ill patients carries a high mortality. Identification and treatment of the underlying etiology simultaneously with prompt therapy are indicated to avoid the consequences of prolonged shock. Physicians should assess patients using all available clinical, radiologic, and laboratory data to avoid the pitfalls associated with use of single measures of regional or global perfusion. Continued evidence of inadequate perfusion despite fluid resuscitation warrants consideration of placement of a pulmonary artery catheter or pharmacologic support of the cardiovascular system. Finally, the dynamic nature of physiology in critically ill patients requires constant patient reassessment and flexibility in treatment to tailor therapy individually as the pathologic state evolves.

Topics: Algorithms; Blood Vessels; Catheterization, Swan-Ganz; Glucocorticoids; Heart; Heart Conduction System; Heart Diseases; Heart Failure; Humans; Myocardial Infarction; Oxygen Consumption; Shock, Cardiogenic; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

After failure of initial external defibrillation, restoration of spontaneous circulation is largely contingent on rapid and effective reversal of myocardial ischemia by both mechanical and pharmacologic means. Despite the introduction of modern cardiopulmonary resuscitation (CPR) more than 35 years ago, its universal acceptance, and its wide implementation, no improvements in outcome excepting early defibrillation have been documented over these many years. The science of CPR therefore is still in its infancy. It was incorrectly assumed that all that needs to be known is known and that the need for scientific research was therefore not apparent. Accordingly, serious resuscitation research was neither encouraged nor equitably supported. The ABCs of CPR currently provide for the establishment of a patent airway (A) and intermittent positive pressure ventilation, preferably with oxygen-enriched air (B). These are to be immediately followed with precordial compression (C). This ordering of priorities, however, is based on consensus rather than objective outcome measurements. The ABCs recently have been seriously challenged on the basis of results of both experimental and clinical studies. Conventional external precordial compression restores systemic blood flow. It may be used by both professional and nonprofessional CPR providers, especially bystanders, because of its apparent simplicity and noninvasiveness. However, manual or mechanical external precordial compression typically generates cardiac outputs that represent less than 30% of normal values. Coronary blood flow, which is critical for restoration of spontaneous circulation, is correspondingly reduced. Accordingly, several alternatives to conventional precordial compression have been proposed with the intent of increasing cardiac output and both coronary and cerebral blood flows. Among the large number of pharmaceutical agents initially recommended for cardiac resuscitation, only agents that produce peripheral vasoconstriction are of proved benefit. Epinephrine has been the preferred vasopressor agent for the management of cardiac arrest for more than 35 years because of its alpha-adrenergic effects. However, the potentially adverse effects of epinephrine are related to its beta-adrenergic inotropic actions. The beta-adrenergic actions account for disproportionate increases in myocardial oxygen consumption with increased severity of myocardial ischemic injury and provocation of ectopic ventricular tac

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Adult; Cardiopulmonary Resuscitation; Electric Countershock; Epinephrine; Extracorporeal Circulation; Heart Arrest; History, 16th Century; History, 18th Century; History, 19th Century; History, 20th Century; History, Ancient; Humans; Myocardial Infarction; Myocardium; Oxygen Consumption; Phenylephrine; Vasoconstrictor Agents; Vasopressins

Neuroendocrine response after acute myocardial infarction (MI) results in activation of the sympathetic nervous system, the renin-angiotensin system, and vasopressin and atrial natriuretic peptide release. The net effect of this response is vasoconstriction, cardiac stimulation and regional flow redistribution that may have a favorable effect in some situations and a deleterious effect in others. The possible adverse effects of vasoconstriction were studied in a Veterans Administration Cooperative Study that evaluated a 48-hour infusion of sodium nitroprusside in the setting of acute MI. In the presence of mild, probably primarily diastolic left ventricular dysfunction, nitroprusside appeared to have an adverse effect on long-term survival. However, in the presence of more severe, probably predominantly systolic dysfunction, nitroprusside had a favorable effect on the prognosis. Therefore, the decision of whether to accept or inhibit neuroendocrine activation in acute MI probably depends on the severity of the disease and the timing of the therapeutic intervals.

Topics: Atrial Natriuretic Factor; Humans; Male; Multicenter Studies as Topic; Myocardial Infarction; Neurosecretory Systems; Nitroprusside; Random Allocation; Renin-Angiotensin System; Vasoconstriction; Vasopressins

Topics: Anti-Bacterial Agents; Blood Transfusion; Cryotherapy; Drainage; Esophageal and Gastric Varices; Esophageal Perforation; Gastrointestinal Hemorrhage; Hemostasis; Hepatic Encephalopathy; Humans; Hypertension, Portal; Intubation, Gastrointestinal; Liver Cirrhosis; Myocardial Infarction; Peptic Ulcer; Pneumonia, Aspiration; Portacaval Shunt, Surgical; Sclerosing Solutions; Therapeutic Irrigation; Ulcer; Vasopressins; Vitamin K

Cardiogenic shock (CS) is the most serious complication of acute myocardial infarction (AMI) with high mortality, and the conventional nursing mode can not meet the clinical needs. Studies have shown that integrated care model has advantages for critical and chronic diseases. However, there is no clinical study to evaluate the clinical efficacy of this nursing model on cardiogenic shock induced by acute myocardial infarction (CS-AMI).. This is a prospective randomized controlled trial to study the clinical efficacy of integrated care combined with vasopressin in the treatment of CS-AMI. Participants will be randomized in a 1:1 ratio to receive integrated care combined with vasopressin in the treatment group and conventional care combined with vasopressin in the control group. The patients will be followed up for 3 months after systematic treatment. Observation indicators include: length of hospital stay, quality of life score, blood pressure level, and nursing satisfaction score. Finally, SPASS 20.0 software will be used for statistical analysis of the data.. This study will evaluate the clinical efficacy of integrated nursing combined with vasopressin in the treatment of CS-AMI. The results of this study will provide a reference for selecting appropriate nursing programs for CS-AMI patients.. OSF Registration number: DOI 10.17605/OSF.IO/K8CN4.

Topics: Delivery of Health Care, Integrated; Humans; Myocardial Infarction; Prospective Studies; Quality of Life; Randomized Controlled Trials as Topic; Shock, Cardiogenic; Treatment Outcome; Vasopressins

To investigate whether sitagliptin affects copeptin and osmolality, suggesting arginine vasopressin activation and a potential for fluid retention, compared with placebo, in patients with a recent acute coronary syndrome and newly discovered type 2 diabetes or impaired glucose tolerance. A second aim was to confirm whether copeptin correlated with insulin-like growth factor binding protein-1.. Fasting blood samples were used from the BEta-cell function in Glucose abnormalities and Acute Myocardial Infarction trial, in which patients recently hospitalized due to acute coronary syndrome and with newly detected abnormal glucose tolerance were randomized to sitagliptin 100 mg once daily (n = 34) or placebo (n = 37). Copeptin, osmolality and insulin-like growth factor binding protein-1 were analysed at baseline and after 12 weeks.. Copeptin and osmolality were unaffected by sitagliptin. There was no correlation between copeptin and insulin-like growth factor binding protein-1.. Sitagliptin therapy does not appear to be related to activation of the arginine vasopressin system.

Topics: Acute Coronary Syndrome; Aged; Aged, 80 and over; Biomarkers; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Double-Blind Method; Drug Administration Schedule; Female; Glycopeptides; Hospitalization; Humans; Insulin-Like Growth Factor Binding Protein 1; Insulin-Secreting Cells; Male; Middle Aged; Myocardial Infarction; Neurophysins; Osmolar Concentration; Protein Precursors; Sitagliptin Phosphate; Sweden; Time Factors; Treatment Outcome; Vasopressins; Water-Electrolyte Balance

The role of the vasopressin system after acute myocardial infarction is unclear. Copeptin, the C-terminal part of the vasopressin prohormone, is secreted stoichiometrically with vasopressin. We compared the prognostic value of copeptin and an established marker, N-terminal pro-B-type natriuretic peptide (NTproBNP), after acute myocardial infarction.. In this prospective single-hospital study, we recruited 980 consecutive post-acute myocardial infarction patients (718 men, median [range] age 66 [24 to 95] years), with follow-up over 342 (range 0 to 764) days. Plasma copeptin was highest on admission (n=132, P<0.001, day 1 versus days 2 to 5) and reached a plateau at days 3 to 5. In the 980 patients, copeptin (measured at days 3 to 5) was elevated in patients who died (n=101) or were readmitted with heart failure (n=49) compared with survivors (median [range] 18.5 [0.6 to 441.0] versus 6.5 [0.3 to 267.0] pmol/L, P<0.0005). With logistic regression analysis, copeptin (odds ratio, 4.14, P<0.0005) and NTproBNP (odds ratio, 2.26, P<0.003) were significant independent predictors of death or heart failure at 60 days. The area under the receiver operating characteristic curves for copeptin (0.75) and NTproBNP (0.76) were similar. The logistic model with both markers yielded a larger area under the curve (0.84) than for NTproBNP (P<0.013) or copeptin (P<0.003) alone, respectively. Cox modeling predicted death or heart failure with both biomarkers (log copeptin [hazard ratio, 2.33], log NTproBNP [hazard ratio, 2.70]). In patients stratified by NTproBNP (above the median of approximately 900 pmol/L), copeptin above the median (approximately 7 pmol/L) was associated with poorer outcome (P<0.0005). Findings were similar for death and heart failure as individual end points.. The vasopressin system is activated after acute myocardial infarction. Copeptin may predict adverse outcome, especially in those with an elevated NTproBNP (more than approximately 900 pmol/L).

Topics: Adult; Aged; Aged, 80 and over; Area Under Curve; Biomarkers; England; Female; Follow-Up Studies; Glycopeptides; Heart Failure; Humans; Kaplan-Meier Estimate; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Peptide Fragments; Prognosis; Proportional Hazards Models; Prospective Studies; Protein Precursors; ROC Curve; Survival Analysis; Treatment Outcome; Ultrasonography; Vasopressins

This study was conducted to evaluate the degree of neurohumoral activation around the time of hospital discharge after myocardial infarction.. Because pharmacologic interventions that block the effects of neurohumoral activation improve the prognosis after infarction, we hypothesized that widespread neurohumoral activation persists in some patients until at least the time of hospital discharge and that the determinants of activation vary from one system to another.. Five hundred nineteen patients in the Survival and Ventricular Enlargement Study (SAVE) had plasma neurohormones measured before randomization at a mean of 12 days after infarction. All patients had left ventricular dysfunction (left ventricular ejection fraction < or = 40%) but no overt heart failure.. Although all neurohormones except epinephrine were increased compared with values in age-matched control subjects, plasma norepinephrine (301 +/- 193 vs. 222 +/- 87 pg/ml, p < 0.001), renin activity (3.0 +/- 3.7 vs. 1.2 +/- 1.2 ng/ml per h, p < 0.001), arginine vasopressin (1.9 +/- 6.9 vs. 0.7 +/- 0.3 pg/ml, p < 0.001) and atrial natriuretic peptide (75 +/- 75 vs. 21 +/- 9 pg/ml, p < 0.001) values ranged from normal to very high, indicating a wide spectrum of neurohumoral activation. Activation of one system did not correlate with activation of another. The clinical and laboratory variables most closely associated with neurohumoral activation were Killip class, left ventricular ejection fraction, age and use of diuretic drugs. The association between neurohumoral activation and clinical and laboratory variables varied from one neurohormone to another.. Neurohumoral activation occurs in a significant proportion of patients at the time of hospital discharge after infarction. Which neurohormone is activated and which clinical and laboratory variables determine this activation vary from one neurohormone to another.

Topics: Aged; Aldosterone; Atrial Natriuretic Factor; Cardiac Output, Low; Dopamine; Female; Humans; Male; Middle Aged; Myocardial Infarction; Neurotransmitter Agents; Norepinephrine; Renin; Stroke Volume; Vasopressins; Ventricular Function, Left

Neuroendocrine response after acute myocardial infarction (MI) results in activation of the sympathetic nervous system, the renin-angiotensin system, and vasopressin and atrial natriuretic peptide release. The net effect of this response is vasoconstriction, cardiac stimulation and regional flow redistribution that may have a favorable effect in some situations and a deleterious effect in others. The possible adverse effects of vasoconstriction were studied in a Veterans Administration Cooperative Study that evaluated a 48-hour infusion of sodium nitroprusside in the setting of acute MI. In the presence of mild, probably primarily diastolic left ventricular dysfunction, nitroprusside appeared to have an adverse effect on long-term survival. However, in the presence of more severe, probably predominantly systolic dysfunction, nitroprusside had a favorable effect on the prognosis. Therefore, the decision of whether to accept or inhibit neuroendocrine activation in acute MI probably depends on the severity of the disease and the timing of the therapeutic intervals.

Topics: Atrial Natriuretic Factor; Humans; Male; Multicenter Studies as Topic; Myocardial Infarction; Neurosecretory Systems; Nitroprusside; Random Allocation; Renin-Angiotensin System; Vasoconstriction; Vasopressins

Intraarterial vasopressin has been reported to be effective in the treatment of massive upper gastrointestinal hemorrhage. A prospective, controlled clinical trial comparing conventional treatment with conventional therapy plus intraarterial vasopressin was undertaken. Sixty episodes of upper gastrointestinal hemorrhage were evaluated during a 40-month period; 32 received conventional and 28 conventional plus vasopressin therapy. The two groups of patients were similar in type and severity of their bleeding lesions and in their underlying diseases. Vasopressin was more effective in controlling hemorrhage from nonvariceal lesions (P less than 0.05) and from varices (P less than 0.01) than conventional therapy. Transfusion requirements were significantly reduced in those patients who received vasopressin. Paradoxically, survival was not affected by vasopressin administration. The failure of cessation of hemorrhage to improve survival is thought to be due to the degree of advancement of the underlying disease, to the torrential nature of the hemorrhage, to the frequency of recurrent hemorrhage, and to the use of intraarterial vasopressin in some patients in the conventional treatment group in whom conventional therapy had failed.

Topics: Adult; Aged; Arrhythmias, Cardiac; Blood Transfusion; Clinical Trials as Topic; Connecticut; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Injections, Intra-Arterial; Long-Term Care; Male; Middle Aged; Myocardial Infarction; Peptic Ulcer Hemorrhage; Placebos; Prognosis; Recurrence; Vasopressins

Acute heart failure (AHF) due to acute myocardial infarction (AMI) is likely to involve cardiogenic shock (CS), with neuro-hormonal activation. A relationship between AHF, CS and vasopressin response is suspected. This study aimed to investigate the implication of vasopressin on hemodynamic parameters and tissue perfusion at the early phase of CS complicating AMI. Experiments were performed on male Wistar rats submitted or not to left coronary artery ligation (AMI and Sham). Six groups were studied Sham and AMI treated or not with either a vasopressin antagonist SR-49059 (Sham-SR, AMI-SR) or agonist terlipressin (Sham-TLP, AMI-TLP). Animals were sacrificed one day after surgery (D

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Heart Failure; Male; Myocardial Infarction; Rats; Rats, Wistar; Shock, Cardiogenic; Stroke Volume; Vasopressins; Ventricular Function, Left

The present study was conducted to identify the effect of vasopressin (AVP) on electrocardiographic changes produced by ischemia-reperfusion. Male rats were divided into seven groups (n=8-13) subjected to 30min ischemia and 120 min reperfusion. In protocol I (control group), saline was administered before ischemia. In protocol II, different doses of AVP (0.015, 0.03, 0.06 and 0.12μg/rat) were infused 10 min before ischemia. In protocol III SR49059 (1 mg/kg), was injected 20 min prior to ischemia with and without the effective dose of AVP (0.03 g/rat). Ischemia-induced arrhythmia and myocardial infarct size (IS) were measured. Different doses of vasopressin decreased IS. There were no significant differences in PR, QRS duration and &DGR;T/amp;DGR;ST ratio between control and intervention groups in ischemia. ST elevation was significantly increased in control and AVP 0.015, 0.03, 0.06 groups during ischemia. In AVP 0.12 group there was no significant difference in ST deviation between the baseline and ischemia phase. JT interval was significantly increased in control and antagonist group during ischemia. AVP 0.12μ/rat prevented the increase of JT interval in ischemia compared to the baseline. In summary, AVP mediated preconditioning improved ST resolution, prevented prolongation of JT interval and decreased the likelihood of subsequently ventricular arrhythmia.

Topics: Animals; Cardiotonic Agents; Dose-Response Relationship, Drug; Electrocardiography; Male; Myocardial Infarction; Myocardial Reperfusion Injury; Rats; Rats, Wistar; Vasopressins

The present study was designed to investigate the mechanisms by which P2X7 receptors (P2X7Rs) mediate the activation of vasopressinergic neurons thereby increasing sympathetic hyperactivity in the paraventricular nucleus (PVN) of the hypothalamus of rats with acute myocardial ischemia (AMI). The left anterior descending branch of the coronary artery was ligated to induce AMI in rats. The rats were pretreated with BBG (brilliant blue G, a P2X7R antagonist), nelivaptan (a vasopressin V1b receptor antagonist), or diphenyleneiodonium (DPI) [an nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor]. Hemodynamic parameters of the heart were monitored. Myocardial injury and cardiomyocyte apoptosis were assessed. In the PVN of AMI rats, P2X7R mediated microglial activation, while reactive oxygen species (ROS) and NADPH oxidase 2 (NOX2) were higher than in the sham group. Intraperitoneal injection of BBG effectively reduced ROS production and vasopressin expression in the PVN of AMI rats. Moreover, both BBG and DPI pretreatment effectively reduced sympathetic hyperactivity and ameliorated AMI injury, as represented by reduced inflammation and apoptosis of cardiomyocytes. Furthermore, microinjection of nelivaptan into the PVN improved cardiac function and reduced the norepinephrine (AE) levels in AMI rats. Collectively, the results suggest that, within the PVN of AMI rats, P2X7R upregulation mediates microglial activation and the overproduction of ROS, which in turn activates vasopressinergic neuron-V1b receptors and sympathetic hyperactivity, hence aggravating myocardial injury in the AMI setting.

Topics: Animals; Myocardial Infarction; Paraventricular Hypothalamic Nucleus; Rats; Reactive Oxygen Species; Receptors, Purinergic P2X7; Sympathetic Nervous System; Vasopressins

Myocardial infarction (MI) is a leading cause of death worldwide. For those who survive the acute insult, the progressive dilation of the ventricle associated with chronic heart failure is driven by an adverse increase in circulating levels of the antidiuretic hormone, vasopressin, which is secreted from hypothalamic supraoptic (SON) and paraventricular nuclei (PVN) nerve terminals. Although increased vasopressin neuronal activity has been demonstrated in the latter stages of chronic heart failure, we hypothesised that vasopressin neurones become activated immediately following an acute MI. Male Sprague-Dawley rats were anaesthetised and an acute MI was induced by ligation of the left anterior descending coronary artery. After 90 minutes of myocardial ischaemia, brains were collected. Dual-label immunohistochemistry was used to quantify the expression of Fos protein, a marker of neuronal activation, within vasopressin- or oxytocin-labelled neurones of the hypothalamic PVN and SON. Fos protein and tyrosine hydroxylase within the brainstem were also quantified. The results obtained show that the expression of Fos in both vasopressin and oxytocin neurones of the PVN and SON was significantly elevated as soon as 90 minutes post-MI compared to sham rats. Moreover, Fos protein was also elevated in tyrosine hydroxylase neurones in the nucleus tractus solitarius and rostral ventrolateral medulla of MI rats than sham rats. We conclude that magnocellular vasopressin and oxytocin neuronal activation occurs immediately following acute MI, rather than in the later stages of chronic heart failure. Therefore, prompt vasopressin antagonist therapy as an adjunct treatment for acute MI may impede the progression of ventricular dilatation, which remains a key adverse hallmark of chronic heart failure.

Topics: Animals; Brain Stem; Coronary Occlusion; Male; Myocardial Infarction; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Proto-Oncogene Proteins c-fos; Rats; Supraoptic Nucleus; Tyrosine 3-Monooxygenase; Vasopressins

Several pieces of evidence indicate that the microglial P2X7 receptor (P2X7R) regulate cardiovascular activities. We explored the possible roles of microglial P2X7R in the PVN mediated sympathoexcitatory responses in acute myocardial infarction (AMI) rat. Sprague-Dawley rats underwent coronary artery ligation to induce AMI. The rats received intraperitoneal administration of the P2X7R antagonist Brilliant Blue-G (BBG, 25 or 50 mg kg(-1), once a day for 5 days) prior to myocardial ischemia. Other rats received bilateral microinjection of P2X7R-siRNA (0.015 or 0.03 nmol 0.1μl per side, once a day for 2 days) targeting P2X7R mRNA into the PVN prior to myocardial ischemia. First, we examined the ATP levels and protein expression P2X7R in the PVN in different ischemia time groups, and we found that the change of P2X7R was positive correlated with the ATP levels in a time-dependent manner. The double-immunofluorescence evidence showed that P2X7R was mainly co-localizated with the microglial marker Iba-1 in the PVN. Second, gene knockdown of P2X7R with P2X7-siRNA or inhibition of P2X7R with BBG reduce the mRNA and protein expression of IL-1β and TNF-α in the PVN of AMI rat. Third, microinjected P2X7-siRNA also suppressed the up-regulation of P2X7R, oxytocin and vasopressin in the PVN of AMI rats. Fourth, P2X7-siRNA and BBG also attenuated the renal sympathetic nerve activity (RSNA) in the AMI rats. Our results indicate that microglial P2X7R activation in PVN mediating the production of proinflammatory cytokines that activate oxytocinergic and vasopressinergic neuron, which augmented the RSNA in the AMI rat.

Topics: Adenosine Triphosphate; Animals; Antigens, Nuclear; Blood Pressure; Calcium-Binding Proteins; Heart Rate; Interleukin-1beta; Male; Microfilament Proteins; Myocardial Infarction; Nerve Tissue Proteins; Oxytocin; Paraventricular Hypothalamic Nucleus; Purinergic P2X Receptor Antagonists; Rats, Sprague-Dawley; Receptors, Purinergic P2X7; RNA, Small Interfering; Rosaniline Dyes; Tumor Necrosis Factor-alpha; Vasopressins

Topics: Animals; Electrocardiography; Glycopeptides; Heart Ventricles; Humans; Male; Myocardial Contraction; Myocardial Infarction; Myocardium; Vasopressins; Ventricular Remodeling

The purpose of the present study was to elucidate if rats with myocardial infarction manifest altered responsiveness to central cardiovascular effects of low doses of angiotensin II (ANG II), and if ANG II and vasopressin (VP) cooperate in the central regulation of cardiovascular functions at rest and during stress. Conscious Sprague-Dawley rats with myocardial infarction induced by left coronary artery ligation, or sham-ligated (SL) controls were infused intracerebroventricularly with artificial cerebrospinal fluid (aCSF), ANG II, ANG II + VP or ANG II + V1a receptor antagonist (V1ANT) 4 weeks after cardiac surgery. In the infarcted but not in the SL rats, the resting mean arterial blood pressure (MABP) was significantly elevated by infusions of ANG II and ANG II + VP, while infusion of ANG II + V1ANT was not effective. During administration of aCSF, the pressor, and tachycardic responses to an air-jet stressor were significantly greater in the infarcted than in the SL rats. In the SL rats, the pressor responses to the stressor were significantly greater during infusions of ANG II, ANG II + VP and ANG II + V1ANT than during infusion of aCSF. The tachycardic response in the SL rats was enhanced only by the combined infusion of ANG II + VP. In the infarcted rats, the pressor and the tachycardic responses to the stressor were similar in all groups. It is concluded that: (1) under resting conditions the infarcted rats manifest sensitisation to the central pressor effect of ANG II and that this effect depends on concomitant stimulation of V1a VP receptors, (2) central ANG II may enhance the pressor response to an alarming stressor in the SL rats through an action which does not depend on the concomitant stimulation of V1a receptors, (3) the cooperative action of ANG II and VP is required for intensification of the tachycardic response to the alarming stressor in the SL rats and (4) exaggeration of the cardiovascular responses to the alarming stressor in the infarcted rats cannot be further augmented by an additional stimulation of central ANG II receptors or combined stimulation of ANG II and VP receptors.

Topics: Angiotensin II; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Blood Pressure; Heart Rate; Injections, Intraventricular; Male; Myocardial Infarction; Rats; Rats, Sprague-Dawley; Stress, Physiological; Vasopressins

Acute myocardial infarction (AMI) is associated with left ventricular (LV) dysfunction and clinical heart failure. Arginine vasopressin is elevated in heart failure and the C-terminal of provasopressin (Copeptin) is associated with adverse outcome post-AMI. The aim of this study was to describe the association between Copeptin with LV dysfunction, volumes, and remodeling and clinical heart failure post-AMI.. We studied 274 subjects with AMI. Copeptin was measured from plasma at discharge and subjects underwent echocardiography at discharge and follow-up (median 155 days). Subjects were followed for clinical heart failure for a median of 381 days. Remodeling was assessed as the change (Delta) in LV volumes between echo examinations. Copeptin correlated directly with wall motion index score (WMIS) and inversely with LV ejection fraction (LVEF) at discharge (WMIS, r=0.276, P < .001; LVEF, r=-0.188, P=.03) and follow-up (WMIS, r=0.244, P < .001; LVEF, r=-0.270, P < .001) and with ventricular volumes at follow-up (LVEDV, r=0.215, P=.002; LVESV, r=0.299, P < .001). Copeptin was associated with ventricular remodeling; DeltaEDV; r=0.171, P=0.015, DeltaESV; r=0.186, P=.008. Subjects with increasing LVESV had higher levels of Copeptin (median 6.30 vs. 5.75 pmol/L, P=.012). Subjects with clinical heart failure (n=30) during follow-up had higher Copeptin before discharge (median 13.55 vs. 5.80, P < .001). In a Cox proportional hazards model, Copeptin retained association with clinical heart failure. Kaplan-Meier assessment revealed increased risk in subjects with Copeptin >6.31 pmol/L.. Copeptin is associated with LV dysfunction, volumes, and remodeling and clinical heart failure post-AMI. Measurement of Copeptin may provide prognostic information and the AVP system may be a therapeutic target in post-MI LV dysfunction.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Female; Follow-Up Studies; Glycopeptides; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Survival Rate; Vasopressins; Ventricular Dysfunction, Left; Ventricular Remodeling

Milrinone used for acute cardiac insufficiency could be of interest during cardiopulmonary resuscitation because of its positive inotropic effects. In this study, the combination of milrinone-vasopressin was compared with epinephrine and vasopressin, as well as with the combination of epinephrine-vasopressin, in reference to hemodynamics.. Thirty-two pigs underwent ligation of the circumflex coronary artery and induction of ventricular fibrillation lasting for 4 min. Cardiopulmonary resuscitation was performed after randomization to one of four groups: epinephrine (30-microg/kg bolus), vasopressin (0.4-U/kg bolus), epinephrine-vasopressin (15-microg/kg epinephrine bolus, 0.2-U/kg vasopressin bolus), or milrinone-vasopressin (0.4-U/kg vasopressin bolus, 50-microg/kg milrinone bolus over 5 min and a continuous infusion of 0.4 microg.kg.min). The hemodynamic variables were measured before cardiopulmonary resuscitation as well as 4, 8, 15, and 30 min after return of spontaneous circulation.. All animals were resuscitated successfully. The animals of the milrinone-vasopressin group displayed significantly (P<0.05) higher cardiac index values (30 min after return of spontaneous circulation: epinephrine, 65.8+/-13.2; vasopressin, 70.7+/-18.3; epinephrine-vasopressin, 69.1+/-36.2; milrinone-vasopressin, 120.7+/-34.8 ml.min.kg) without a decrease in mean arterial pressure or coronary perfusion pressure.. The combination of vasopressin-milrinone as compared with epinephrine during cardiopulmonary resuscitation leads to an improved cardiac index without relevant decrease of mean arterial pressure or coronary perfusion pressure.

Topics: Animals; Blood Pressure; Cardiopulmonary Resuscitation; Coronary Circulation; Disease Models, Animal; Drug Therapy, Combination; Male; Milrinone; Myocardial Infarction; Phosphodiesterase Inhibitors; Swine; Vasopressins

Left ventricular end-diastolic pressure (LVEDP) during exercise workload is an important parameter to guide an exercise prescription for patients with cardiovascular disease. Plasma levels of neuro-hormonal factors can be used as a reflection of real-time LVEDP, but its utility is limited by its short half-life. By contrast, the N-terminal fragment of pro-ANP (NT-ANP) has a longer half-life of 1 h.. To determine whether plasma NT-ANP levels at 30 min after exercise can be used as a marker of LVEDP during peak exercise workload in patients with previous myocardial infarction.. Twenty patients with a previous history of myocardial infarction.. Cardiopulmonary exercise test was performed to determine peak VO(2) and anaerobic threshold. Plasma levels of ANP, BNP, NT-ANP, vasopressin and plasma catecholamine were measured at rest, maximum exercise, and 30 min after exercise (recovery).. With the exception of NT-ANP, the levels of each of neuro-hormonal factors peaked at maximum exercise and returned to baseline at recovery. By contrast, NT-ANP levels also increased at peak exercise but remained elevated at 30 min after exercise. Furthermore, NT-ANP levels at recovery correlated with ANP levels at maximum exercise (p<0.01, R=0.75), left ventricular ejection fraction (p<0.02, R=-0.54) and left ventricular systolic dimension (p<0.015, R=0.50).. Plasma NT-ANP levels at 30 min after exercise reflect ANP levels at maximum exercise and left ventricular overload during exercise. These data indicate that plasma NT-ANP after exercise may be a useful parameter to guide prescription of cardiac rehabilitation.

Topics: Aged; Atrial Natriuretic Factor; Blood Pressure; Catecholamines; Exercise; Female; Half-Life; Humans; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Oxygen Consumption; Peptide Fragments; Protein Precursors; Time Factors; Vasopressins; Ventricular Dysfunction, Left

Blindness caused by ischemic optic neuropathy in the hospital setting occurs perioperatively and in critically ill patients, but its etiology remains ill defined. We describe four critically ill patients who developed blindness within 1 mo of one another. Three cases occurred outside of the operative arena. Potential risk factors for the development of ischemic optic neuropathy, such as use of vasopressors, venous congestion, and hypotension, are described.

Topics: Accidents, Traffic; Blindness; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Diverticulitis; Female; Flail Chest; Hemothorax; Humans; Intensive Care Units; Lung Injury; Male; Middle Aged; Myasthenia Gravis; Myocardial Infarction; Optic Nerve Injuries; Optic Neuropathy, Ischemic; Pancreatitis; Pelvic Bones; Prone Position; Risk Factors; Sepsis; Spinal Fractures; Vasopressins

In a retrospective study of 36 patients who developed cardiogenic shock after myocardial infarction, intravenous vasopressin therapy increased mean arterial pressure from 56 to 73 mm Hg at 1 hour (p < 0.001) and maintained it for 24 hours without changing pulmonary capillary wedge pressure, cardiac index, urine output, or other inotropic requirements. After norepinephrine administration, mean pulmonary capillary wedge pressure increased at 1 hour from 21 to 24 mm Hg (p = 0.04); however, this increase was not sustained at 12 and 24 hours. Norepinephrine was associated with a significant increase in cardiac power index at 24 hours, whereas there was only a trend for an increase in cardiac power with vasopressin therapy. In a cohort of patients who developed refractory cardiogenic shock after myocardial infarction, vasopressin was associated with increased mean arterial pressure and no adverse effect on other hemodynamic parameters.

Topics: Aged; Blood Pressure; Cardiac Output; Female; Follow-Up Studies; Humans; Male; Myocardial Infarction; Norepinephrine; Pulmonary Wedge Pressure; Retrospective Studies; Shock, Cardiogenic; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Stress is one of the factors provoking cardiovascular complications. The purpose of the study was to explore the role of vasopressin (VP) in central control of arterial blood pressure and heart rate under resting conditions and during stimulation by an alarming stress (air jet stress) in myocardial infarct-induced cardiac failure. Six groups of male Sprague Dawley (SD) rats were subjected either to sham surgery (sham rats) or to ligation of a left coronary artery (infarcted rats). After 5 weeks both infarcted and sham rats were subjected either to intracerebroventricular infusion of artificial cerebrospinal fluid (aCSF) (sham aCSF and infarcted aCSF), [Arg8]-VP (sham VP and infarcted VP) or VP V1a receptor antagonist (d(CH2)5[Tyr(Me)2Ala-]VP, sham V1ANT and infarcted V1ANT). Air jet stress elicited significantly greater increases in mean arterial blood pressure (MABP) and heart rate in the infarcted aCSF than in the sham aCSF rats. Intracerebroventricular infusion of V1ANT significantly reduced resting MABP and MABP and heart rate increases in response to stress in the infarcted but not in the sham rats. Intracerebroventricular infusion of VP elicited a significant increase in resting MABP in the infarcted VP but not in the sham VP rats. The results provide evidence for enhanced engagement of the brain V1 VP receptors in regulation of resting MABP and in generation of exaggerated cardiovascular responses to air jet stress during the post-infarct state.

Topics: Animals; Blood Pressure; Brain; Cardiovascular System; Heart Rate; Male; Models, Cardiovascular; Myocardial Infarction; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Stress, Physiological; Vasopressins

Myocardial infarction is usually induced in small animals by means of invasive procedures: the aim of this study was to cause heart necrosis lesions by non-invasive means. We injected rabbits with isoproterenol (3 mg/kg, i.p.) and vasopressin (0.3 mg/kg/5 min, i.v.) alone and in combination, and studied their effects on myocardial histology, electrocardiographic profiles, the appearance of the plasma cardiac necrosis marker c-troponin I (c-TPN I), hemodynamic parameters (blood pressure, heart rate), the coagulative process partial throboplastine time (PTT), and plasma nitric oxide (NO) levels. In the rabbits treated with vasopressin alone, the ischemic damage was associated with a decrease in NO values, and the appearance of electrocardiographic T-wave inversion and low plasma c-TPN I levels, whereas the animals treated with isoproterenol alone had necrotic bands in the myocardium, plasma c-TPN I, and electrocardiographic modifications (ST-segment changes and T-wave inversion). Combined treatment increased myocardial alterations such as contraction band necrosis, induced the appearance of specific hypoxic lesions such as areas of coagulative necrosis and leukocyte infiltration, and led to higher plasma c-TPN I levels and altered ECG profiles. Both drugs favored a decrease in plasma NO values and further alterations in hemodynamic parameters, such as higher blood pressure and greater procoagulant activity. The myocardial necrosis and modified cardiovascular parameters were attributed to calcium activated processes and the decrease in NO levels. As this model of myocardial damage involves the use of drugs that facilitate the opening of L-calcium channels, we also investigated their effects on cardiovascular parameters and heart histology after pretreatment with the calcium antagonist verapamil; this drug protected against the appearance of histological myocardial lesions, electrocardiographic alterations and high plasma c-TPN I levels, and prevented the hemodynamic and procoagulation changes, but did not affect the decrease in plasma NO values. The protective effects were attributed to the drug's calcium antagonist activity. In conclusion, the injection of isoproterenol and vasopressin induces a myocardial infarction non-invasively and seems to be suitable for studying early myocardial ischemic lesions and the effects of drugs interfering with myocardial damage and its related phenomena.

Topics: Animals; Blood Pressure; Calcium Channel Blockers; Disease Models, Animal; Electrocardiography; Heart Rate; Isoproterenol; Male; Myocardial Infarction; Myocardium; Nitric Oxide; Partial Thromboplastin Time; Rabbits; Sympathomimetics; Troponin I; Vasoconstrictor Agents; Vasopressins; Verapamil

Impaired regulation of salt and water balance in left ventricular dysfunction and heart failure can lead to pulmonary and peripheral edema and hyponatremia. Previous studies of disordered water regulation in heart failure have used models of low cardiac output with normal cardiac function (e.g., inferior vena cava ligation). We investigated thirst and vasopressin (AVP) secretion in a rat myocardial infarction model of chronic left ventricular dysfunction/heart failure in response to a 24-h water deprivation period. Thirst (implied from water drunk), hematocrit, plasma renin activity, and plasma AVP concentrations increased with water deprivation vs. ad libitum water access. Thirst and plasma AVP concentrations were significantly positively correlated with infarct size after 24-h water deprivation but not under ad libitum water access conditions. The mechanism by which this occurs is unclear but could involve increased osmoreceptor sensitivity, altered stimulation of baroreceptors, the renin-angiotensin system, or altered central neural control.

Topics: Animals; Body Weight; Disease Models, Animal; Heart Failure; Myocardial Infarction; Organ Size; Rats; Rats, Sprague-Dawley; Thirst; Vasopressins; Ventricular Dysfunction, Left; Water Deprivation; Water-Electrolyte Balance

Myocardial infarction often induces congestive heart failure accompanied by a significant increase in plasma vasopressin concentration. To delineate the role of vasopressin in the pathogenesis of congestive heart failure, the acute hemodynamic and aquaretic effects of conivaptan (YM087, 4'-(2-methyl-1,4,5,6-tetrahydroimidazo[4,5-d][1]benzoazepine-6-carbonyl)-2-phenylbenzanilide monohydrochloride), a combined vasopressin V(1A) and V(2) receptor antagonist, were assessed in rats with heart failure induced by myocardial infarction. Left coronary artery ligation resulted in decreased left ventricular systolic pressure and first derivatives of left ventricular developed pressure, as well as increased left ventricular end-diastolic pressure, lung and right ventricular weight. Single oral administration of conivaptan (0.3 to 3.0 mg/kg) dose-dependently increased urine volume and decreased urine osmolality in heart failure rats. Furthermore, conivaptan (3.0 mg/kg) attenuated the changes in left ventricular end-diastolic pressure, lung and right ventricular weight induced by heart failure while reducing blood pressure. These results show that vasopressin plays a significant role in elevating vascular tone through vasopressin V(1A) receptors and plays a major role in retaining free water through vasopressin V(2) receptors in this model of congestive heart failure. Additionally, conivaptan, with its dual vasopressin V(1A) and V(2) receptor-inhibiting properties, could exert a beneficial effect on cardiac function in the congestive heart failure rat model.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Dose-Response Relationship, Drug; Heart Failure; Hemodynamics; Male; Myocardial Infarction; Rats; Rats, Wistar; Vasopressins

The effects of SMP-300, an orally active, potent, and selective Na+/H+ exchange inhibitor, were evaluated and compared with those of nifedipine, propranolol, and nicorandil on three experimental angina models and on myocardial infarction in rats. SMP-300 (0.1-1 mg/kg, p.o.) reduced isoproterenol-induced ST segment depression in a dose-dependent manner. Its maximal effect was comparable to that reported for propranolol and greater than that of nifedipine. SMP-300 (0.3-1 mg/kg) reduced vasopressin-induced ST segment depression in a dose-dependent manner, and its maximal effect was comparable to those of nifedipine and nicorandil. SMP-300 (0.3-1 mg/kg, p.o.) and propranolol (100 mg/kg, p.o.) inhibited coronary artery occlusion-induced T-wave elevation, but nifedipine (3 mg/kg, p.o.) did not. SMP-300 (1 mg/kg, p.o.) reduced myocardial infarct size after 40 min of coronary artery occlusion followed by 24 h of reperfusion, but nifedipine (3 mg/kg, p.o.) or propranolol (100 mg/kg, p.o.) did not. This study provides support for the future use of a Na+/H+ exchange inhibitor as an anti-anginal drug with a novel mode of action.

Topics: Administration, Oral; Angina Pectoris; Animals; Azocines; Coronary Disease; Electrocardiography; Isoproterenol; Male; Myocardial Infarction; Myocardial Reperfusion Injury; Myocardium; Nicorandil; Nifedipine; Propranolol; Pyrroles; Rats; Rats, Sprague-Dawley; Rats, Wistar; Sodium-Hydrogen Exchangers; Vasodilator Agents; Vasopressins

Acute myocardial infarction evokes activation of, among others, the arginine-vasopressin system, resulting in vasoconstriction and fluid retention. In the present study, the vasoconstrictor and antidiuretic effects of vasopressin were examined in vivo in conscious rats with chronic myocardial infarction, in the absence or presence of the V(1a) receptor antagonist SR-49059 or the V(2) receptor antagonist OPC-31260. In sham rats, vasopressin dose-dependently increased mean arterial pressure (maximum response: 45+/-3 mm Hg), which was significantly suppressed in infarcted rats (maximum response: 32+/-3 mm Hg). SR-49059, but not OPC-31260, caused a significant rightward shift of the dose pressure response curve in sham rats, indicating V(1a) receptor mediation. This rightward shift by SR-49059 was significantly more in infarcted rats. The suppressed response to the agonist and enhanced sensitivity to the antagonist suggest a reduction of V(1a) receptor number in infarcted rats. In both sham and infarcted rats, the urine production after OPC-31260 (337+/-14 and 329+/-30 microl/min, respectively) was about twice of that in vehicle-treated rats (188+/-25 and 155+/-24 microl/min, respectively). However, the response in infarcted rats reached its peak quicker and lasted for a shorter period, resulting in a 40% lower area under the curve. Although only measurable during V(2) receptor blockade, the reduction of urine production by vasopressin was significantly more in infarcted compared to sham rats. The enhanced renal response to the agonist and reduced response to the antagonist suggest an increase in V(2) receptor number in infarcted rats. In conclusion, in chronically infarcted rats, vasopressin causes vasoconstriction and fluid retention through the V(1a) and V(2) receptors, respectively. Altered responses after infarction indicate a shift from V(1a) to V(2) receptors.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Blood Pressure; Chronic Disease; Consciousness; Coronary Vessels; Dose-Response Relationship, Drug; Indoles; Kidney; Ligation; Male; Myocardial Infarction; Pyrrolidines; Rats; Rats, Wistar; Receptors, Vasopressin; Urination; Urodynamics; Vasopressins

A patient with perforated appendicitis developed progressive vasodilatory shock which was complicated by perioperative acute myocardial infarction. Cardiovascular support included dopamine infusion, and later, intra-aortic balloon counterpulsation balloon pump and noradrenaline and dobutamine infusion. Vasopressin was introduced as a final attempt to reverse the refractory shock and was associated with recovery. The experience with this case suggests that vasopressin may be a valuable adjunct to the treatment of catecholamine-resistant vasodilatory shock.

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Aged; Appendicitis; Cardiotonic Agents; Dobutamine; Dopamine; Humans; Infusions, Intravenous; Intestinal Perforation; Intra-Aortic Balloon Pumping; Intraoperative Complications; Male; Myocardial Infarction; Norepinephrine; Recovery of Function; Shock; Vasoconstrictor Agents; Vasodilation; Vasopressins

This study was designed to assess the effect of a nonpeptide vasopressin V1-receptor antagonist, OPC-21268, and a vasopressin V2-receptor antagonist, OPC-31260, on hemodynamics in the early phase and the late phase after myocardial infarction in rats. In the early phase, OPC-21268 (30 mg/kg/day) or OPC-31260 (30 mg/kg/day) was orally administered from day 1 to day 5 after the operation; and hemodynamics were measured at day 5, in the late phase from 10 weeks to 11 weeks and measured at the end of 11 weeks. In the early phase, OPC-21268 reduced the left ventricular end-diastolic pressure (LVEDP) concomitantly with the reduction in systemic blood pressure, but did not change LVEDP in the late phase. OPC-31260 reduced LVEDP and central venous pressure in both phases. OPC-21268 improved hemodynamics only in the early phase and OPC-31260 improved it in both phases.

Topics: Administration, Oral; Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Heart Ventricles; Hemodynamics; Male; Myocardial Infarction; Organ Size; Piperidines; Quinolones; Rats; Rats, Wistar; Time Factors; Vasopressins; Ventricular Function, Left

Remodelling after myocardial infarction (MI) is associated with vascular adaption, increasing vascular capacity of non-infarcted myocardium, and angiogenesis in the infarcted part during wound healing and scarring. We investigated regional vascular reactivity in the infarcted rat heart. Transmural infarction of the left ventricular free wall was induced by coronary artery ligation. After 3 weeks, regional flow during maximal vasodilation (nitroprusside, NPR) and submaximal vasoconstriction (arginine-vasopressin, AVP) were studied in buffer-perfused hearts. The main findings were: (1) a reduced vasodilator response (NPR) in the viable part of the left ventricular free wall, where hypertrophy was most pronounced, resulting in reduced maximal tissue perfusion of the myocardium bordering the scar (19.7 + 0.6 v 25.7 + 1.2 ml/min.g), whereas perfusion of other non-infarcted regions was preserved. (2) A 54% lower vasodilator response (NPR) and a 25% stronger vasoconstriction (AVP) in scar tissue compared to viable parts of MI hearts. Microscopy showed thicker walls of resistance arteries in scar tissue than in viable parts of MI hearts or in sham hearts, morphometrically substantiated by two- to three-fold greater wall/lumen ratios. These data indicate a deviant response of scar vessels of MI hearts, and in the non-infarcted part, a reduced coronary reserve in the most hypertrophied region. Whereas the former may be caused by different vessel structure, the reduced vasodilator reserve of the spared part of the left ventricular free wall may indicate vasodilation at rest due to insufficient vascular growth. Thus, the most hypertrophied region would be at the highest risk of further ischemic damage.

Topics: Animals; Cicatrix; Coronary Circulation; Coronary Vessels; Heart; Male; Myocardial Infarction; Nitroprusside; Organ Size; Rats; Rats, Wistar; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

In this study, the model of early myocardial infarction (EMI) was produced by legation of left anterior descending artery in rat. The artery spasm (CAS) was produced by external jugular vein injection of vasopressin (VP). Myocardium of apex and adjoining slice was used to make paraffin sections, then HE and LSAB-Mb staining were performed. Results showed: In 25 min after myocardial infarction, stretch-shape Mb depletion was observed in subendocardial myocardium of aortic ventricle's frontal wall. As the time of EMI prolonged, stretch-shape Mb depletion extended to epicardial layer. In CAS group, multiply, spotty Mb depletion was detected. There were more Mb depletion zones in right heart than that in left heart. The Mb depletion zones surrounded the CA or were like grape-clusters along the branches of one large CA. Thus, myocardial Mb depletion induced by EMI and CAS had different morphologic peculiarity. LSAB-Mb method could be hoped for the use of supplying objectively morphologic evidence to myocardial ischemia induced by CAS.

Topics: Animals; Coronary Vasospasm; Myocardial Infarction; Myocardium; Myoglobin; Rats; Rats, Wistar; Vasopressins

Experimental myocardial infarction is a model of cardiac overload in which part of the cardiac muscle is removed. The resulting left ventricle insufficiency depends on the size of the infarct and time. The infarcted area remodels, due to proteolytic activity of inflammatory cells and collagenogenesis from fibroblast activity. The phenotype of the residual healthy cardiac muscle undergoes modification, and there are peripheral vascular changes which are partly dependent on the activation of pressor systems and/or inactivation of dilator systems. The changes are proportional to the infarct size at any given time after induction of the model. The degree of right ventricular hypertrophy and the drop in arterial pressure are upstream and downstream markers of the loss of left ventricular function and therefore indicate the extent of the remodelling. The increase of type V3isomyosin, the amount of subendocardial collagen, and the biosynthesis, storage and secretion of atrial natriuretic factor (ANF) are all proportional to the infarct size and the degree of cardiac overload. The level of urinary cGMP is also correlated with infarct size. These indices show ventricular remodelling, increased stress and energy restriction of the residual healthy cardiac muscle. The activation of peripheral pressor systems also depends on infarct size. They reflect the influence of defective cardiac pumping on the kidney, liver, brain and endothelium. Massive infarcts are accompanied by an increase in circulating renin and in renal renin content, by a decrease in angiotensinogen due to its consumption by renin, and to its insufficient hepatic synthesis, and by an increase in vasopressin secretion and biosynthesis in the hypothalamus. Converting enzyme inhibition has beneficial effect in this model by lowering cardiac load. It reduces arterial pressure, reverses bi-atrial and right ventricular hypertrophy, reduces the changes in the myosin isoenzyme patterns, and normalizes subendocardial fibrosis and the level of ANF. Although the effects of converting enzyme inhibition are beneficial in this model, they are restricted by their inability to normalize the load and stress when the initial loss of cardiac contractile material exceeds 40%.

Topics: Angiotensin-Converting Enzyme Inhibitors; Angiotensinogen; Animals; Atrial Natriuretic Factor; Collagen; Cyclic GMP; Hypertrophy, Left Ventricular; Indoles; Isoenzymes; Kidney; Myocardial Infarction; Myocardium; Myosins; Perindopril; Rats; Rats, Wistar; Renin; Vasopressins; Ventricular Dysfunction, Left

Topics: Adult; Cervix Uteri; Drug Administration Routes; Female; Humans; Intraoperative Complications; Myocardial Infarction; Vasopressins

The purpose of this study was to investigate whether neurohumoral activation occurs in asymptomatic patients with acute myocardial infarction (AMI) and without clinical signs of heart failure. During the early phase of AMI (mean 8 days), the neurohumoral profiles of 60 patients (mean age 59 range 37 to 70) were examined. Blood levels of the following humoral parameters were measured: atrial natriuretic peptide (ANP), plasma renin activity, aldosterone and vasopressin. All patients underwent cardiac catheterization during hospitalization. Baseline hemodynamic characteristics identified left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mmHg) in 32 patients; the remaining 28 patients had normal hemodynamic parameters. In patients with AMI, plasma ANP levels differed significantly from control subjects (111 +/- 74 pg/ml vs. 53 +/- 18 pg/ml; P < 0.001). In patients with AMI and mild left ventricular dysfunction ANP levels were significantly increased when compared to patients with AMI and normal left ventricular function (129 +/- 73 pg/ml vs. 82 +/- 69 pg/ml; P < 0.001). The hemodynamic data showed a significant correlation with ANP only in patients with AMI and left ventricular dysfunction (EF% r = 0.42; LVEDP r = 0.44; P < 0.001). These data show that in patients with myocardial infarction and without heart failure, the atrial natriuretic peptide is the only neurohumoral system activated out of all neurohumoral systems tested in this population and its circulating levels are strictly related to the degree of left ventricular dysfunction.

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Female; Humans; Male; Middle Aged; Myocardial Infarction; Renin; Stroke Volume; Vasopressins; Ventricular Function, Left

Plasma atrial natriuretic factor (ANF) levels were measured in 29 patients who had normal atrial hemodynamics on days 4 and 8 after an uncomplicated acute myocardial infarction (AMI). All patients had increased ANF levels on day 4. On day 8 of the ANF levels had declined significantly to normal values in 14 patients with enzymatically smaller AMI and higher ejection fractions (> or = 40%), while they remained elevated in 16 patients with larger AMI and lower ejection fractions (< 40%). The study data are compatible with increased secretion of ANF by the more extensively damaged left ventricles in AMI.

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Prospective Studies; Renin; Vasopressins; Ventricular Function, Left

Topics: Female; Humans; Hypertension, Portal; Injections, Intravenous; Middle Aged; Myocardial Infarction; Syndrome; Vasopressins

The purpose of the present study was to measure plasma levels of atrial natriuretic peptide (ANP) in patients with acute myocardial infarction without heart failure, and also to assess the temporal sequence of changes of plasma ANP during the first hours of recovery from myocardial infarction. The study was performed in 22 patients who were admitted to the Intensive Care Unit with the diagnosis of acute myocardial ischaemia that had an evolution of less than 6 h. Blood samples were drawn on admission and at 1, 8, and 24 h, and plasma concentrations of ANP, renin, aldosterone, epinephrine, norepinephrine and vasopressin were measured. Compared with control subjects, on admission patients showed increased plasma levels of ANP, as well as increased plasma renin activity (PRA), aldosterone, norepinephrine, epinephrine, dopamine, and antidiuretic hormone (ADH). ANP, but not renin or aldosterone plasma values, decreased with time, and there was a significant correlation between ANP and time after onset of pain. No increase in plasma creatinine was observed during the hospital stay, and the patients showed a negative fluid balance. No relationship was found between the location or extension of the infarction, or morphine treatment and ANP plasma levels. The high levels of ANP seem to counteract the haemodynamic and fluid-retention effects of the vasoconstrictive factors released after myocardial infarction.

Topics: Aldosterone; Analysis of Variance; Atrial Natriuretic Factor; Catecholamines; Female; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Regression Analysis; Renin; Time Factors; Vasopressins

Topics: Blood Loss, Surgical; Coronary Artery Bypass; Humans; Myocardial Infarction; Thrombosis; Vasopressins

Plasma atrial natriuretic factor, aldosterone, renin activity, and antidiuretic hormone were studied in low output heart failure syndromes: cardiogenic shock in ten patients with acute myocardial infarction of the anterior wall (first group), hypovolemic shock after melena from peptic ulcer in ten subjects (second group), and hypotension with bradycardia syndrome in ten patients with acute myocardial infarction of the inferior wall (third group). Circulating atrial natriuretic factor in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) was significantly higher than in healthy volunteers matched for sex and age (8.4 +/- 0.3 pg/ml). In these patients there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the second and third groups were within normal range. Plasma aldosterone was high in all groups, plasma renin activity was elevated in the first and third groups, and high antidiuretic hormone was observed in the first and second groups. These findings indicate that in low output heart failure syndromes only hemodynamic changes affecting the atria stimulate atrial natriuretic factor release. No correlations were found between plasma atrial natriuretic factor and other hormones. In particular, high atrial natriuretic factor levels in the patients with cardiogenic shock did not inhibit release of aldosterone, renin, or antidiuretic hormone. It may be surmised that in these patients the hemodynamic effects override the inhibitory effects of atrial natriuretic factor.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Blood Volume; Bradycardia; Cardiac Output, Low; Female; Heart Failure; Humans; Male; Melena; Middle Aged; Myocardial Contraction; Myocardial Infarction; Peptic Ulcer Hemorrhage; Renin; Shock, Cardiogenic; Vascular Resistance; Vasopressins; Venous Pressure

Plasma atrial natriuretic factor (ANF), renin activity (PRA), aldosterone and antidiuretic hormone (ADH) were determined in 16 patients with uncomplicated acute myocardial infarction (AMI) for 7 days in all patients and in six patients for 8 more days. Echocardiograms were performed and central venous pressure (CVP) was measured on the 2nd, 7th and 15th days. On admission, plasma ANF was higher in patients with AMI (129.8 +/- 70.6 pg ml-1, mean +/- SD) than in healthy volunteers (50.6 +/- 10.0 pg ml-1) (P less than 0.05). Arterial pressure, heart rate, CVP were normal. Left atrial (LAD) and left ventricular diameters (LVDD) were increased in six patients. Ejection fraction (EF) was reduced in all. A significant inverse relationship between ANF and EF was observed. Patients with EF less than or equal to 45%, high LAD and LVDD had the highest plasma ANF and showed steady high plasma ANF for 15 days. Patients with EF greater than 45%, normal LAD and LVDD had elevated plasma levels only for 10 days, rising significantly on days 3-7 after admission. PRA and ADH values were normal throughout the study, whereas aldosterone was above the normal range only on admission. These findings suggest that the reduction in myocardial contractility induced by the infarction may account for the rise in ANF secretion via increased left atrial pressure or left atrial dilatation.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Renin; Stroke Volume; Vasopressins

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Bradycardia; Cardiac Output, Low; Female; Hemodynamics; Humans; Hypotension; Male; Middle Aged; Myocardial Infarction; Renin; Shock; Shock, Cardiogenic; Vasopressins

Topics: Aged; Gastrointestinal Hemorrhage; Humans; Infusions, Intravenous; Male; Myocardial Infarction; Vasopressins

The pituitaries and adrenals of 30 patients died from extensive fresh myocardial infarction and of 25 patients died from other diseases were studied. In myocardial infarction the mean weight of the above glands was significantly higher than in other diseases. In most cases an increase in number of pituitary ACTH-cells was observed with the immunoperoxidase method. In non-cardiogenic shock (another 9 cases) gland weight was also increased but without a significant increase in the number of ACTH-cells. Hyperactivity of the anterior pituitary-adrenal system is due to a number of known factors. It may be assumed that patients who have infarction are either exposed to an extraordinary amount of stress stimuli or are more susceptible to stress than normal subjects. The findings may indicate the morphological basis of this situation. Of the shock phenomena, incomplete necrosis and haemorrhage of the adrenal cortex are frequent. In the pituitary neural lobe the neurosecretory material, which proved to be vasopressin with the PAP-method, was found to be increased more frequently in myocardial infarction than after other diseases.

Topics: Adrenal Cortex; Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; Female; Humans; Immunoenzyme Techniques; Male; Middle Aged; Myocardial Infarction; Organ Size; Pituitary Gland, Anterior; Shock; Shock, Cardiogenic; Vasopressins

Since current data on vasopressin (AVP) secretion during the early phase of myocardial infarction is not extensive, plasma AVP was measured in 26 patients with acute myocardial infarction. Twelve had an increased AVP concentration (23.2 +/- 7.0 pg/ml; mean +/- SEM) whereas 14 had an AVP level less than 3 pg/ml (1.96 +/- 0.14 pg/ml). The patients with AVP greater than 3 pg/ml had higher heart rate and plasma osmolality than those with AVP less than 3 pg/ml. Blood pressure values were the same in both groups of patients. There was no difference in peak CPK and iso CPK activities between the two groups. Seven patients with AVP greater than 3 pg/ml died within the next few days, while only 1 patient with AVP less than pg/ml died. It thus appears that increased AVP concentration during acute myocardial infarction is associated with a poor prognosis. Whether it is a cause or a consequence of an unfavourable course of myocardial infarction remains to be determined.

Topics: Adult; Aged; Aged, 80 and over; Female; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Vasopressins

Earlier we have shown in the dog model mimicking angina on effort a delayed antiischaemic effect of PgI2 and its stable analogue 7-oxo-PgI2-Na, appearing only when the drug induced marked vasodilatation was over [1]. In the present experiments we could show that the protective effect appears at a time when the blood pressure returned to normal and in addition the marked platelet aggregation inhibitory effect has also faded away. In the rat 7-oxo-PgI2 could substantially diminish vasopressine induced T-wave elevation in the ECG if given 2 hours before administration of vasopressin. In addition it could moderate the vasopressin induced metabolic changes appearing as diminution of the myocardial CP and ATP-level and increase of the myocardial lactate content. A similar metabolic protection was found in the heart of rats pretreated with 7-oxo-PgI2 2 hours before taking myocardial samples and exposing them for 1 minute to ischaemia by incubation in Ringer solution. It is concluded that a direct metabolic and hemodynamic effect could be at least partly responsible for the late antiischaemic effect of 7-oxo-PgI2. This effect was also present in the early phase of experimental myocardial infarction in conscious rats if animals were pretreated with 7-oxo-PgI2 2 hours before occlusion. However treatment did not increase survival rate and failed to reduce the incidence and severity of arrhythmias.

Topics: Adenine Nucleotides; Angina Pectoris; Animals; Disease Models, Animal; Dogs; Epoprostenol; Female; Heart; Lactates; Male; Myocardial Infarction; Myocardium; Phosphocreatine; Rats; Rats, Inbred Strains; Vasopressins

Most patients with upper gastrointestinal hemorrhage from Mallory-Weiss tear cease bleeding spontaneously and do not require specific therapy. Patients who either continue to bleed and those who rebleed represent specific therapeutic problems. Angiotherapy, either intraarterial vasopressin infusion (13 cases) or arterial embolization (two cases), was used to treat 15 patients with persistently bleeding Mallory-Weiss tears. Permanent hemostasis was achieved in the majority of patients treated. Results from the current study are compared with those previously reported in the literature. In addition the complications of each treatment method are discussed with emphasis on the cardiac complications of vasopressin.

Topics: Adolescent; Adult; Aged; Embolization, Therapeutic; Female; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Male; Mallory-Weiss Syndrome; Middle Aged; Myocardial Infarction; Postoperative Complications; Retrospective Studies; 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

A new rapid method for producing myocardial necrosis in rabbits was developed, using percutaneous intramyocardial injection of vasopressin in peanut oil. The 15-min procedure resulted in a mortality rate of 15% and a success rate among surviving animals of 50%. When the lesions were 24 hr old, strontium-85 and a technetium-99m-tagged agent were injected intravenously simultaneously, and the animals were killed 1,6, and 24 hr later for tissue radioassay. Strontium-85 failed to accumulate appreciably in the lesions. Three bone-seeking technetium complexes (pyrophosphate, methylene diphosphonate, and imidodiphosphonate) produced lesion-to-normal myocardial ratios of 6,5, and 14, respectively, at 1 hr, and 20,30, and 33 at 6 hr. The ratios for 99mTc-glucoheptonate were only 2 at 1 hr and 4 at 6 hr, while the ratios of 99mTc-acetylcysteine and 99mTc-citrate were even lower.

Topics: Animals; Citrates; Cysteine; Diphosphates; Diphosphonates; Disease Models, Animal; Myocardial Infarction; Rabbits; Radionuclide Imaging; Strontium Radioisotopes; Sugar Acids; Technetium; 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

The hypothalamo-hypophyseal neurosecretory system (HHNS) was studied in patients dying at various intervals after the onset of the first clinical manifestations of myocardial infarction. All the 75 cases were divided into two groups depending on the presence or absence of decompensation with disorders of the water-salt metabolism. Despite the duration and pattern of its course, myocardial infarction was shown to be always accompanied by a high activity of the HHNS and adrenal cortex, although different variants of its intensity could be distinguished by the studies of the secretory cycle in neurosecretory nuclei. When infarction was complicated by cardiac decompensation, there developed the state of hypervasopressinism constantly accompanied by hyperthrophy of the glomerular zone of the adrenal cortex producing aldosteron and by an increased concentration of intracellular sodium.

Topics: Adrenal Cortex; Aldosterone; Cell Nucleus; Dihydrolipoamide Dehydrogenase; Glutamate Dehydrogenase; Humans; Hypothalamo-Hypophyseal System; Hypothalamus; Myocardial Infarction; Neurons; Pituitary Gland, Posterior; Vasopressins

Topics: Afferent Pathways; Angiotensin II; Animals; Arteries; Blood Circulation; Blood Pressure; Cardiovascular Physiological Phenomena; Chemoreceptor Cells; Coronary Circulation; Efferent Pathways; Heart; Humans; Hypothalamus; Myocardial Contraction; Myocardial Infarction; Pressoreceptors; Pressure; Reflex; Renin; Spinal Cord; Sympathetic Nervous System; Vagus Nerve; Vasomotor System; Vasopressins

Trapymin (TM) relaxed excised renal, coronary, pulmonary, femoral and mesenteric arteries and this relaxation was not antagonized by propranolol. The dose-response curve of TM was parallel to that of nitroglycerin and papaverine and steeper than that of dipyridamol or adenosine. TM exerted inotropic and chronotropic actions on excised rat atrium. TM was also effective through the oral route and the effectiveness tended to decrease slightly after repeated use for ten days. TM was effective on vasopressin induced angina in rats and electrocoagulation-induced myocardial infarction. TM suppressed adrenaline-induced arrhythmia but not CaCl2-induced arrhythmia. TM reduced catecholamine content in brain, adrenals and heart but had no influence on monoamine oxidase or dopamine-beta-hydroxylase. TM revealed ganglion-blocking and neuron-blocking actions in cervical ganglion in cats. With propranolol, TM-induced hyperglycemia and reduction in glycogen content in liver and heart was antagonized but TM-induced rise in free fatty acid in serum was not antagonized. Na+-K+ dependent ATPase of bovine heart and P/O ratio of mitochondria of rat heart was not influenced by TM. ADP-induced aggregation of platelets was antagonized by TM. These data indicate that TM induced coronary dilation is partly due to a papaverine like action and also to ganglion-blocking, neuron-blocking and anti-adrenergic action. On the other hand, TM possessed catecholamine release and cardiotonic action as related to beta-receptors.

Topics: Adenosine Triphosphate; Animals; Arrhythmias, Cardiac; Blood Glucose; Calcium Chloride; Catecholamines; Cats; Cattle; Coronary Circulation; Dopamine beta-Hydroxylase; Epinephrine; Female; Glycogen; In Vitro Techniques; Isoproterenol; Male; Monoamine Oxidase; Myocardial Contraction; Myocardial Infarction; Myocardium; Platelet Aggregation; Propranolol; Pyrimidines; Rabbits; Rats; Trapidil; Vasodilator Agents; Vasopressins

Topics: Angiotensin II; Animals; Arrhythmias, Cardiac; Coronary Vessels; Dogs; Drug Hypersensitivity; Epinephrine; Female; Hypersensitivity, Delayed; Hypersensitivity, Immediate; Male; Myocardial Infarction; Norepinephrine; Vasopressins

Topics: Aminocaproates; Animals; Arrhythmias, Cardiac; Benzoates; Myocardial Infarction; Rats; Vasopressins

Topics: Aminocaproates; Animals; Arrhythmias, Cardiac; Benzoates; Myocardial Infarction; Rabbits; Rats; Vasopressins

Topics: Adult; Chlorpropamide; Diabetes Insipidus; Female; Humans; Injections, Intramuscular; Male; Middle Aged; Myocardial Infarction; Polyuria; Vasopressins

Topics: Animals; Colloids; Coronary Disease; Coronary Vessels; Dextrans; Electrocardiography; Erythrocyte Aggregation; Myocardial Infarction; Rabbits; Vasopressins

Topics: Adenosine Triphosphate; Animals; Aspartic Acid; Electrocardiography; Glucose; Insulin; Male; Myocardial Infarction; Potassium; Rabbits; Vasopressins

Topics: Animals; Aortic Diseases; Atropine; Dogs; Electrocardiography; Epinephrine; Heart Auscultation; Heart Sounds; Hemodynamics; Hemorrhage; Histamine; Infusions, Parenteral; Isoproterenol; Methoxamine; Myocardial Infarction; Norepinephrine; Pharmacology; Phenylephrine; Phonocardiography; Pulmonary Artery; Research; Respiration; Vascular Diseases; Vasopressins; Venae Cavae; Veratrine

Topics: Amino Alcohols; Amyl Nitrite; Animals; Anti-Arrhythmia Agents; Arginine Vasopressin; Ballistocardiography; Dogs; Epinephrine; Myocardial Infarction; Pharmacology; Quinidine; Renin; Tetraethylammonium Compounds; Vasopressins

Topics: Arginine Vasopressin; Epinephrine; Humans; Hypersensitivity; Myocardial Infarction; Serum Sickness; Vasopressins

Topics: Cardiovascular Diseases; Heart; Humans; Myocardial Infarction; Pituitary Gland; Pituitary Hormones; Vasopressins

Topics: Cholecystography; Death, Sudden; Electrocardiography; Heart; Humans; Infarction; Myocardial Infarction; Pituitary Gland; Pituitary Hormones; Vasopressins

Topics: Androgens; Atropine; Cardiovascular Diseases; Heart; Infarction; Myocardial Infarction; Pituitary Diseases; Pituitary Gland; Pituitary Hormones; Testosterone; Vasopressins