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)

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.
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PMID:[Pharmacology of cornary dilator agent, trapymin. (2) Analysis of its mode of action]. 124 70

Once the bleeding patient has been resuscitated and the diagnosis of acute variceal hemorrhage established by endoscopy, emergency injection sclerotherapy should be employed as the therapeutic option of choice. Endoscopic band ligation is a promising new technique that may prove to be as effective as sclerotherapy, with fewer complications. Pharmacologic treatment (with vasopressin and nitroglycerin) and balloon tamponade remain important alternative treatments, both as empiric temporizing therapy before sclerotherapy can be arranged and in the approximately 30% of patients who continue to bleed after a single sclerotherapy session. Continued bleeding in many of these patients can be controlled with a second session of sclerotherapy. If active acute bleeding persists after two sclerotherapy treatments, treatment should be considered a failure. Some of these patients may be suitable for surgical treatment with either staple-gun transection of the esophagus or emergency portacaval shunting.
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PMID:Treatment of acute variceal bleeding. 134 2

Successful pharmacological arrest of haemorrhage might avoid the risk of aspiration associated with tamponade and early studies have suggested that the vasoactive agent somatostatin may be as effective and perhaps safer than tamponade in controlling variceal haemorrhage. In our view, vasopressin has not established a role in management but we retain an open mind regarding the potential use of terlipressin in combination with nitroglycerin. It is unlikely that any of these agents can improve significantly our ability to control variceal haemorrhage when compared to balloon tamponade but they may reduce the incidence of pulmonary complications and thereby reduce subsequent mortality. Tamponade has proved successful in controlling acute haemorrhage from oesophageal varices in our hands. Late complications continue to give cause for concern but until effective safe alternatives to tamponade are developed, we continue to advocate its use for emergency control of acute variceal haemorrhage. Our own studies have shown that the high mortality seen in this patient population may reflect the severity of the underlying liver disease rather than failure of a management policy employing oesophageal tamponade for the initial control of acute variceal haemorrhage.
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PMID:Balloon tamponade and vasoactive drugs in the control of acute variceal haemorrhage. 135 76

Although the mechanism initiating and maintaining variceal hemorrhage is not completely understood, there has been general agreement in recent years on the concept that variceal rupture occurs when the tension on the wall of the varices reaches a critical value (the rupture point) that leads to the leakage of the elastic components of the wall. If this hypothesis is true, the aim of pharmacological treatment should be to reduce variceal wall tension or to prevent any abrupt increase in this parameter. Some vasoconstrictor drugs are currently used in order to achieve these goals and in the attempt to stop the acute bleeding episode. All these agents decrease either portal pressure and azygos blood flow. Vasopressin although effective, has significant cardiac and gastrointestinal adverse effects that discourage its use. Combination with nitroglycerin reduces its adverse effects while maintaining or even enhancing the reduction in portal pressure. Glypressin, which acts as a slow-release preparation of vasopressin, has a longer duration of action and can be administered as single intravenous injections instead of continuous infusion. However, the similarity of effects of these drugs on systemic circulation leads to an overlapping spectrum of untoward effects. Somatostatin and the synthetic octapeptide octreotide display similar pharmacological effects on splanchnic hemodynamics but have a better tolerability profile. Thanks to its longer duration of action and ease of administration, octreotide could become the drug of choice for the early, pre-hospital management of bleeding varices. A different approach to the pharmacological treatment of variceal bleeding may be the use of compounds, like metoclopramide and domperidone, that increase the lower esophageal sphincter pressure (LESP), thereby reducing the inflow of blood flow into the submucous venous plexus of the esophagus and hence into the esophageal varices. However, more studies are needed before these compounds be considered a real alternative to the above established drugs.
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PMID:Clinical pharmacology of active variceal bleeding. 136 76

Vasoactive drug therapy is the only therapy that can be administered immediately to patients with suspected variceal bleeding. The optimal agent is not yet available, but somatostatin or octreotide, glypressin and vasopressin and nitroglycerin are the best candidates. Somatostatin and octreotide have the best therapeutic index as they have very few side effects. They compare well to the other agents in comparative randomized trials. In addition to being used prior to sclerotherapy, vasoactive agents may show benefit when used in combination with endoscopic methods and in the immediate interval thereafter in order to prevent early re-bleeding. This remains to be tested in clinical trials.
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PMID:Medical management of bleeding esophageal varices. 136 77

Variceal bleeding is the most important complication of portal hypertension. Mortality due to the first variceal bleeding is very high (50%) and of those surviving a variceal bleeding episode, up to 80% may rebleed. Proper management of the acute variceal bleeding episode, the prevention of rebleeding and primary prophylaxis for variceal haemorrhage are therefore mandatory in order to improve the morbidity and mortality of cirrhotic patients with variceal bleeding. Injection sclerotherapy would be the treatment of choice for acute variceal bleeding. Drug treatment in the form of either a combined vasopressin-nitroglycerin regimen or somatostatin may be used as an alternative. Patients not responding to these treatments should be referred for surgery. For the prevention of variceal rebleeding, non-selective beta-blockers should be tried first, reserving long-term injection sclerotherapy for patients with contraindications or intolerance to beta-blockers or in whom beta-blocker therapy has failed. Surgical rescue in the form of either shunt surgery or lever transplantation should be considered if either treatment fails. A new technique, transjugular intrahepatic portosystemic stent-shunt (TIPSS) may replace shunt surgery in the future. Beta-blockers is the treatment of choice for primary prophylaxis of variceal haemorrhage and has a role in preventing acute and chronic bleeding from congestive gastropathy. However, the above sequential approach from the least invasive to the more invasive therapeutic options may not be appropriate for all cirrhotic patients with variceal bleeding.
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PMID:Management of variceal haemorrhage. 136 89

Following the demonstration that somatostatin lowered portal pressure in cirrhotic patients with portal hypertension, 2 uncontrolled reports suggested that the hormone might be useful in the control of acute variceal haemorrhage. Subsequently, a number of randomised controlled trials have indicated that somatostatin may have an efficacy as good as or better than either vasopressin or combined vasopressin and nitroglycerin therapy and is associated with fewer side effects. Somatostatin has an efficacy comparable to balloon tamponade, histamine-2-receptor antagonists and injection sclerotherapy. One double-blind randomised controlled trial demonstrated a significant benefit of somatostatin over placebo in the control of variceal bleeding whereas a second did not show any significant difference between treatments. In all the controlled trials, the average control rate achieved with somatostatin administration was 69% and it was not associated with any major side effects. Somatostatin administration has also been shown in uncontrolled series to be very effective in controlling postinjection sclerotherapy bleeding from the varices per se, and from oesophageal ulcers and oesophagitis. Few data are available on the long acting analogue of somatostatin, octreotide, but preliminary data suggest that it may be as effective and safe as the native hormone in controlling the acute variceal bleeding and postinjection sclerotherapy haemorrhage. It is concluded that there may be a case for instituting somatostatin therapy as soon as the patient enters hospital to facilitate sclerotherapy, and for continuing treatment for 5 days after sclerotherapy when the risk of recurrent bleeding is highest.
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PMID:Somatostatin in acute bleeding oesophageal varices. Clinical evidence. 138 69

Terlipressin (Glypressin), a synthetic analog of vasopressin, induces arteriolar vasoconstriction which causes both a portal hypotensive effect and certain side-effects on the systemic circulation (elevated arterial pressure and reduced cardiac output). The combination of nitroglycerin with terlipressin might accentuate the portal hypotensive effect and prevent the side-effects on the systemic circulation. The aim of this study was to examine the systemic and splanchnic hemodynamic responses to terlipressin administered alone or combined with nitroglycerin in patients with cirrhosis. Systemic and splanchnic hemodynamics were measured before and 1 h after a bolus of terlipressin (1 to 2 mg IV) given alone (n = 10) or in association with nitroglycerin infusion (25 micrograms/min, n = 9). Terlipressin alone significantly increased the arterial pressure by 21%, systemic vascular resistance by 60%, and significantly decreased cardiac output by 23%. The right atrial and pulmonary pressures significantly increased and the wedged hepatic venous pressure and hepatic venous pressure gradient significantly decreased by 8% and 16%, respectively. The combined therapy decreased the cardiac output by 20%, but did not significantly modify the other systemic and splanchnic hemodynamic values. No significant differences were found between terlipressin and the combined therapy concerning changes in wedged hepatic venous pressure or hepatic venous pressure gradient. We conclude that in patients with cirrhosis, nitroglycerin prevents the deleterious vasoconstrictor and vasopressor effects of terlipressin. However, the combined therapy, as terlipressin alone, decreases the cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic effects of the administration of terlipressin alone or combined with nitroglycerin in patients with cirrhosis]. 142 24

A 70-yr-old male presented with massive upper gastrointestinal bleeding secondary to esophageal varices. Because the bleeding was not controlled by sclerotherapy or vasopressin and nitroglycerin, the patient was evaluated for a transjugular intrahepatic portosystemic shunt. Preprocedure arteriography was performed because the etiology of the portal hypertension was uncertain. The arteriogram revealed a hepatic artery to portal vein fistula. Hepatic venous pressure measurements documented an elevated hepatic venous pressure gradient, which diminished dramatically upon embolization of the fistula. Rebleeding from the varices was associated with reestablishment of the fistula via collaterals and elevation of the hepatic venous pressure gradient. The case is presented to establish a role for arteriography prior to transjugular intrahepatic portosystemic shunting, especially in patients with unexplained portal hypertension, and to establish the potential value of hepatic venous pressure measurements in the treatment of arterioportal fistulas.
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PMID:Arterioportal fistula: a role for pre-TIPSS arteriography and hepatic venous pressure measurements. 144 52

Ischemia and reperfusion alter the reactivity of large coronary arteries, but the effect of ischemia and reperfusion on the coronary microcirculation has been less well defined. Elevated circulating levels of vasopressin are associated with cardiopulmonary bypass and numerous other clinical states in which vascular ischemia and reperfusion may occur. We examined the effects of ischemia with and without reperfusion on the responses to vasopressin of both large coronary arteries and coronary arterial microvessels. Studies were performed on vessels from control dogs (n = 8), dogs undergoing 1 hour of ischemia only (n = 8), and dogs undergoing 1 hour of ischemia followed with 1 hour of reperfusion (n = 9). Rings of proximal obtuse marginal coronary arteries distal to the site of circumflex coronary artery occlusion were studied in isolated organ chambers. Coronary microvessels (110 to 220 microns in diameter) were studied in a pressurized (20 mm Hg), no-flow state with a microvessel imaging apparatus and electronic dimension analyzer. Microvessels were preconstricted with the thromboxane A2 analog U46619. Responses of large vessel rings were studied in the nonpreconstricted state and after preconstriction with prostaglandin F2 alpha. Large vessel response to vasopressin was minimal and not altered by ischemia with or without reperfusion. In contrast, ischemia markedly affected the coronary microvascular response to vasopressin (10 to 1000 microU/ml). Control coronary microvessels constricted minimally to vasopressin (4% +/- 2% of the baseline diameter), while microvessels after either ischemia alone or ischemia followed by reperfusion constricted 22% +/- 5% and 21% +/- 3%, respectively (p less than 0.05 versus control for both). Hemoglobin, which inactivates the endothelium-derived relaxing factor, augmented microvascular constrictions to vasopressin in all groups to a similar extent. Relaxations to the endothelium-independent agent nitroglycerin were not altered by ischemia. Constrictions of the coronary microcirculation to vasopressin in conditions such as cardiopulmonary bypass or myocardial ischemia, in which circulating levels of vasopressin are increased, may predispose to persistent myocardial ischemia in the perioperative setting.
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PMID:Altered effects of vasopressin on the coronary circulation after ischemia. 149 97


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