Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin has been used with increasing frequency to control gastrointestinal bleeding, the beneficial effect being attributed to marked splanchnic vasoconstriction. Because vasopressin may result in impaired cardiac function and because other potent vasoconstrictive substances have been shown to increase the pulmonary shunt and decrease arterial oxygenation, this study was undertaken to determind the effect of vasopressin on oxygen availability. Ten healthy anesthetized mechanically ventilated dogs received a five hour intravenous vasopressin infusion, 0.005 U/kg/min. The heart rate decreased moderately and briefly. The mean systemic arterial pressure increased and then decreased, both minimally. The pulmonary shunt and the arterial oxygen content decreased slightly. The total systemic resistance increased and the stroke volume decreased, both substantially. The pulmonary artery wedge pressure gradually increased. The oxygen availability decreased markedly. This study demonstrated that a vasopressin infusion causes a marked decrease in oxygen availability due primarily to a decreased stroke volume and, to a lesser extent during the first hour, to a decreased heart rate. The pulmonary shunt did not increase. Increased systemic resistance followed by a gradual increase in the pulmonary wedge pressure suggests that the decreased stroke volume resulted, at least in part, from an increased afterload and left ventricular failure. It is suggested that until the effect of vasopressin on the cardiopulmonary systems and hence oxygen availability is fully studied in critically ill patients, that it be used with caution and with appropriate hemodynamic monitoring.
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PMID:The effect of vasopressin on oxygen availability. 44 98

The systemic and regional hemodynamic effects of arginine vasopressin receptor antagonism (AVPA) and angiotensin-converting enzyme inhibition (ACEi) were examined in rabbits with acute left ventricular failure induced by repetitive direct current (DC) shock. Hemodynamic measurements in 24 rabbits 24 h after DC shock compared with 6 sham-operated controls demonstrated a lowered cardiac output (602 +/- 26 vs. 920 +/- 35 ml/min, P less than 0.01), increased left ventricular end-diastolic pressure (LVEDP, 13.6 +/- 1.3 vs. 1.9 +/- 0.5 mmHg, P less than 0.01) and a raised peripheral resistance (9,734 +/- 495 vs. 6,479 +/- 305 dyn.s.cm-5, P less than 0.01). Cerebral blood flow was not altered in rabbits with acute left ventricular failure but intestinal (29 +/- 2 vs. 53 +/- 9 ml/min, P less than 0.01) and renal (82 +/- 6 vs. 130 +/- 8 ml/min, P less than 0.01) blood flows were significantly reduced. No hemodynamic changes were observed after AVPA alone in the acute heart failure group and ACEi alone reduced LVEDP and increased renal vascular conductance. Treatment with both drugs (i.e., AVPA + ACEi) resulted in a significant increase in cardiac output (21%) and a decrease in blood pressure (19%) and peripheral resistance (34%) and restored renal and intestinal blood flows to near normal levels. Thus both vasopressin and angiotensin contribute to the overall increase in peripheral resistance in this model and to the decrease in intestinal and renal blood flow observed. Presumably blockade of one system produced little hemodynamic change because of compensatory increases in the other system.
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PMID:Systemic and regional effects of vasopressin and angiotensin in acute left ventricular failure. 182 56

A number of theoretical and practical aspects of acute myocardial infarction suggest a potential role for ACE inhibition in enhancing coronary blood flow and limitation of infarct size. Indeed, the use of ACE inhibitors in acute myocardial infarction could be viewed as a logical intervention in the face of the neuroendocrine response which accompanies the acute phase. During the first 24 h post-infarction, very high plasma concentrations of arginine-vasopressin and catecholamines occur. This is followed by a sharp rise in the concentration of angiotensin II (ANG II) over the next few days. The neuroendocrine response is most marked in those patients with larger infarcts, who frequently develop left ventricular failure. The extent to which these factors influence coronary flow in acute myocardial infarction is unknown, although in chronic heart failure ACE inhibition does not reduce coronary blood flow despite a reduction in rate-pressure product, suggesting a coronary vasodilator effect. However, in the presence of fixed coronary stenoses, the fall in blood pressure and, therefore, of coronary perfusion pressure must be taken into account. Whether or not the use of ACE inhibitors can limit infarct size in man also remains to be determined, although it has been clearly demonstrated that concentrations of ANG II similar to those observed in the early phase of myocardial infarction can cause myocardial cell damage in experimental animals. Post-infarction ventricular enlargement can be reduced by ACE inhibitors. Additionally, ACE inhibitors, through their balanced vasodilator effect, maintain cardiac output whilst reducing filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of angiotensin-converting enzyme inhibition on coronary blood flow and infarct size limitation. 267 35

In chronic cardiac failure, various neurohumoral mechanisms are activated to sustain blood volume, blood pressure, and organ perfusion. Using the coronary artery ligation model of heart failure in the rat, we have measured changes in vasoactive hormone secretion and related these changes to salt and water status during a 1-month period. When compared with controls, rats with infarction had a marked rise in plasma atrial natriuretic peptide (294 +/- 59 vs. 79 +/- 10 pg/ml, p less than 0.001) although there was no increase in total exchangeable body sodium. Plasma renin activity and plasma aldosterone concentrations were the same for both rats with infarction and controls. Similarly, there were no significant differences in plasma arginine vasopressin, plasma osmolality, or plasma sodium concentration in rats with infarction. Ventricular norepinephrine levels were reduced in animals with infarction (p less than 0.01). Plasma atrial natriuretic peptide levels were raised in this model of chronic left ventricular failure. However, there was no salt retention and little stimulation of the renin-angiotensin-aldosterone system or vasopressin. The results suggest that high circulating atrial natriuretic peptide levels may prevent or limit salt and water retention, either directly or indirectly, by inhibiting the renin-angiotensin-aldosterone system.
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PMID:Neurohumoral responses to chronic myocardial infarction in rats. 289 63

The role of atrial natriuretic peptide in the pathophysiology of heart failure is unknown. The aim of the study were changes of atrial natriuretic peptide, hemodynamic, renal and hormonal parameters during the development of cardiac failure in an animal model of congestive heart failure in the conscious dog due to rapid right ventricular pacing and in rats with chronic left ventricular failure due to a left ventricular infarction. The effects of intravenous administration of atrial natriuretic peptide were studied in patients with severe congestive heart failure, dogs with experimental cardiomyopathy and conscious rats with acute right ventricular failure due to repeated pulmonary emboli. The results suggest an important role of atrial natriuretic peptide in the early phase of heart failure as a counterregulating system concerning vasoconstrictory and volume retaining mechanisms like the renin-angiotensin-aldosterone system, the sympathetic nerve activity and vasopressin. In chronic heart failure the renal effects of atrial natriuretic peptide are attenuated. Pharmacological doses have beneficial effects on ventricular function by reducing pre- and afterload. The reduction in effectiveness of atrial natriuretic peptide in congestive heart failure may be due to a down-regulation of specific receptors, or caused by hemodynamic renal changes preventing the action of the hormone on the kidney in heart failure or may be due to an activation of counterregulating systems overridding the effects of atrial natriuretic peptide.
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PMID:[Atrial natriuretic peptide in cardiac insufficiency]. 296 47

The present trial compared the effectiveness and complications of intravenous somatostatin and vasopressin in treatment of variceal bleeding. Sixty-one cirrhotic patients with endoscopically proven active variceal bleeding were included. Both drugs were given as continuous intravenous infusions for 48 hr. Thirty patients received somatostatin (250 micrograms per hr after a bolus of 50 micrograms) and 31 vasopressin (0.4 units per min). Initial control of bleeding was achieved in 26 (87%) patients receiving somatostatin and in 23 (74%) of those treated with vasopressin. However, 10 patients [not significant statistically] in the somatostatin group and 5 in the vasopressin group rebled during treatment, after a mean of 15 and 20 hr, respectively. Therefore, complete control of bleeding during the 48 hr of therapy was achieved in 16 (53%) patients treated with somatostatin and in 18 (58%) of those receiving vasopressin. Mortality during hospitalization was similar in both groups (somatostatin 47%, vasopressin 45%). Differences were observed in complications associated with each therapy. Vasopressin produced major complications in 8 patients (left ventricular failure in 4 and severe abdominal pain requiring drug withdrawal in 4), and minor complications in 14; somatostatin infusion produced minor complications in 3 patients (p less than 0.01). In addition, the serum sodium concentration was significantly reduced by vasopressin (from 134.3 +/- 1.6 to 128.3 +/- 1.4 mEq per liter, p less than 0.001) but not by somatostatin (134.6 +/- 1.1 vs. 133.2 +/- 1.1 mEq per liter). This study shows that somatostatin is as effective as vasopressin in controlling variceal hemorrhage, but has a much lower rate of complications.
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PMID:Comparison of intravenous somatostatin and vasopressin infusions in treatment of acute variceal hemorrhage. 614 25

1. The effects of prolonged chlorothiazide treatment of left ventricular failure on cardiac hypertrophy, circulating vasoactive hormones and exchangeable body sodium were examined in rats with chronic myocardial infarction induced by left coronary artery ligation. Chlorothiazide therapy commenced either immediately or 2 weeks after infarction. For 4 weeks, the rats were given either chlorothiazide (50 mg day-1 kg-1) in their drinking water or drinking water alone. 2. Cardiac weight increased in untreated rats with infarction in comparison with sham-operated controls, indicating the presence of chronic left ventricular dysfunction, although exchangeable body sodium, plasma renin activity, plasma vasopressin and plasma osmolality remained unchanged. 3. Chlorothiazide raised haematocrit and plasma renin activity equally in rats with and without infarction, although exchangeable body sodium, plasma vasopressin and plasma osmolality were not changed by the treatment. Plasma atrial natriuretic peptide was 2-fold higher in rats with infarction and this response was not affected by chlorothiazide treatment. Chlorothiazide therapy did not prevent or reverse cardiac hypertrophy. 4. Chronic diuretic therapy in this experimental model of heart failure did not reduce extracellular sodium, plasma vasopressin or the extent of ventricular hypertrophy, possibly because the condition was associated with activation of the renin-angiotensin system.
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PMID:Cardiomegaly and vasoactive hormones in rats with chronic myocardial infarction: long-term effects of chlorothiazide. 869 3

Myocardial ischemia results in myocardial dysfunction. Recovery may be delayed ("stunning"), or persistent if perfusion remains reduced ("hibernation") and ischemia may go on to necrosis, thus, contributing to chronic heart failure. In addition, myocardium not directly affected by ischemia may undergo adaptive processes like hypertrophy and dilatation, which may result in chronic left heart failure. This process is characterized by hemodynamic, neurohumoral, and progressive morphologic changes of the heart which are closely interrelated. Hemodynamic changes basically consist of an increase in left ventricular filling pressure and a decrease in global ejection fraction, and, in most cases years after myocardial infarction, in an increase in systemic vascular resistance and right atrial pressure. Neurohumoral changes consist of an increase in plasma catecholamines, atrial natriuretic factor and vasopressin, and in an activation of the renin-angiotensin-system. Plasma endothelin-1 was recently reported to be increased in patients with heart failure, and prognosis was related to endothelin levels. Diminished response of vessels to endothelium (EDRF/NO) dependent vasodilatation suggests impairment of vascular endothelium in heart failure. Local changes of cardiac neurohumoral systems could contribute to structural changes of the heart, e.g., systemic activation to hemodynamic changes. Structural changes of the heart are characterized by an increase in volume and thickness of surviving myocardium and an expansion of ischemic and necrotic myocardium. Molecular control of these processes which include various cell types, such as cardiomyocytes and cardiofibroblasts, are currently an issue of intense research and could result in specific therapeutic importance.
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PMID:[Transition of myocardial ischemia to heart failure]. 981 48

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ss-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.
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PMID:Congestive heart failure: what should be the initial therapy and why? 1472 93

Experiments in Cape Town in the 1980s demonstrated that acute brain death is followed by massive catecholamine release resulting in systemic hypertension, acute left ventricular failure, and multiple cardiac arrhythmias along with substantial decreases in cortisol, insulin, thyroid, and antidiuretic hormone levels, a change from aerobic to anaerobic metabolism, and increases in inflammatory cytokines. Hormonal replacement results in rapid recovery of cardiac function in both experimental animals and humans and enables significantly more organs to be transplanted. Organ Procurement and Transplantation Network/United Network for Organ Sharing multivariate studies on hormonal treatment of brain-dead donors revealed significant increases in organs transplanted and in one-year survival of kidneys and hearts.
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PMID:Hormonal therapy of the brain-dead organ donor: experimental and clinical studies. 1716 4


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