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)

We sought to determine whether streamlining of portal venous blood occurs in normal anaesthetized rats under basal conditions and with variations in hepatic blood flow. We catheterized the ileocolic vein and injected 15 micron microspheres labeled with 85Sr and 141Ce into this vein and into the spleen, respectively. The hepatic lobar distribution of microspheres was studied in a group under basal conditions and after hepatic blood flow was increased (infusions of nitroglycerin or glucagon) or decreased (infusion of vasopressin or ligation of the superior mesenteric artery); this blood flow was measured with a constant infusion of indocyanine green. Measured results (expressed as proportion of total liver counts per minute) were compared with a reference group in which the portal vein of rats had been partially ligated 10 days prior to study and in which similarly injected microspheres that lodged in the liver were assumed to be completely mixed with portal blood. No differences were seen within groups and between the reference and experimental groups. We conclude that under these experimental conditions, portal venous blood flow appears to be distributed homogeneously between hepatic lobes.
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PMID:Distribution of portal blood flow in the liver of the rat: a microsphere study. 643 27

Nitroglycerin was administered with vasopressin to prevent adverse effects. Vasopressin 0.25U . 70 kg-1 min-1 was infused intravenously in four dogs for 40 minutes, when a venous infusion of nitroglycerin 1.2 micrograms . kg-1 . min-1 was added for 20 minutes. Nitroglycerin 1.2 micrograms . kg-1 . min-1 alone was infused intravenously in another four dogs for 40 minutes. The venous blood pressures (mesenteric and central) and arterial pressures (mesenteric and femoral), the electrocardiogram and arterio-venous difference were recorded. Nitroglycerin was shown to annul the unfavourable effects of vasopressin without altering its efficacy upon portal pressure.
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PMID:Correction of the unfavourable effects of vasopressin by nitroglycerin infusion. 680 67

This study was designed to investigate whether the addition of nitroglycerin to vasopressin infusion could avoid the deleterious systemic effects of vasopressin while maintaining or enhancing the therapeutic benefits of portal pressure reduction. The effect of nitroglycerin on splanchnic and systemic hemodynamics was studied in cirrhotic patients and portal hypertensive dogs receiving i.v. vasopressin. During i.v vasopressin infusion (0.4 units per min), the cardiac output decreased in patients by 14% from 7.6 +/- 0.9 (mean +/- S.E.) to 6.5 +/- 0.7 liters per min, p less than 0.01, the mean arterial pressure increased 21% from 87 +/- 2 to 105 +/- 4, p less than 0.01, and the heart rate decreased 11% from 79 +/- 3 to 71 +/- 3, p less than 0.01. The administration of sublingual nitroglycerin (0.4 mg) returned all the systemic hemodynamic parameters to baseline values. In dogs, vasopressin infusion significantly reduced portal pressure and flow while increasing portal venous resistance. Nitroglycerin when added to the vasopressin infusion reduced portal venous resistance and further decreased portal pressure in dogs. In patients, vasopressin reduced the hepatic blood flow (44%), wedged hepatic venous pressure (11%), and the gradient between wedged and free hepatic venous pressures (23%). Nitroglycerin administration caused a further reduction of the wedged hepatic venous pressure (23.6 +/- 2.3 to 21.1 +/- 2.0, 11%, p less than 0.01). There was a small but not significant further decline (7%) in the hepatic venous pressure gradient. These results provide evidence that the addition of nitroglycerin to an i.v. infusion of vasopressin reversed the detrimental effects of vasopressin while preserving the beneficial effects.
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PMID:Nitroglycerin improves the hemodynamic response to vasopressin in portal hypertension. 681 44

Drug therapy for acute variceal bleeding should be viewed as an adjunct to emergency sclerotherapy. Its role in preventing very early rebleeding (within days) following sclerotherapy needs to be established. The best candidates for such a role are somatostatin and octreotide, but glypressin and vasopressin and nitroglycerin combinations have therapeutic effects in the short-term. Propranolol is the drug for long-term prevention of rebleeding and prevention of the first variceal bleed. For primary prophylaxis it significantly reduces the rate of bleeding, and there is a trend towards reducing mortality. It should be used in cirrhotic patients with large varices. For secondary prophylaxis, propranolol significantly reduces rebleeding but does not improve survival. The reduction in rebleeding is similar to long-term sclerotherapy when compared in randomized studies. There is no value in adding beta-blockers to sclerotherapy compared with sclerotherapy alone, but few studies have evaluated the effects after the eradication of varices. beta-Blockers can be used as the first-line therapy to prevent variceal rebleeding. They also have been shown to reduce the frequency of rebleeding from congestive gastropathy. Many patients do not have a portal pressure reduction with propranolol. The addition of isosorbide mononitrate converts many nonresponders to responders. Current clinical trials are evaluating if therapeutic efficacy is improved by these drug combinations.
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PMID:Pharmacological therapy for portal hypertension: rationale and results. 755 72

Torsade de pointes is an unusual life-threatening ventricular arrhythmia that has been associated with vasopressin, neuroleptic drugs, and electrolyte imbalances, including hypokalemia and hypomagnesemia. Over a 9-month period, we observed torsade de pointes in three patients with cirrhosis and bleeding esophageal varices who did not have prior cardiac disease. All had received endoscopic sclerotherapy and continuous infusions of vasopressin and nitroglycerin. For sedation, two patients received haloperidol and one droperidol. In addition, two patients had either hypokalemia or hypomagnesemia. In all three patients, there was prolongation of the electrocardiographic QT interval and a "long-short" initiating sequence followed by ventricular tachycardia with torsade de pointes morphology. All were successfully cardioverted; there was one late death due to aspiration and septicemia. We conclude that cirrhotics with variceal hemorrhage may be at increased risk of developing this arrhythmia in the setting of treatment with vasopressin, sedation with neuroleptic drugs, and electrolyte abnormalities. We urge close monitoring of these patients for cardiac arrhythmia and recommend that neuroleptics be used cautiously, if at all.
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PMID:Torsade de pointes complicating the treatment of bleeding esophageal varices: association with neuroleptics, vasopressin, and electrolyte imbalance. 773 96

The task of pharmacotherapy in acute haemorrhage from oesophageal varices in patients with cirrhosis of the liver and portal hypertension is to arrest bleeding by reducing the blood pressure and blood flow in the oesophageal varices. The mechanism of action of the majority of drugs used is vasoconstriction of the arterioles in the splanchnic region. Somatostatin seems to be more effective and in particular safer than vasopressin, terlipressin or their combination with the vasodilatator nitroglycerin. Initial pharmacotherapy for rapid control of haemorrhage is simple and effective treatment, however, it cannot be considered an alternative of sclerotherapy, which remains the method of choice in acute haemorrhage from oesophageal varices and is effective in 90-95%. Pharmacotherapy is useful also in the prevention of relapsing haemorrhage from oesophageal varices. A combination of sclerotherapy with somatostatin or nitrates to reduce early relapses of haemorrhage is particularly effective. The effectiveness of beta-blockers to reduce the risk of relapsing haemorrhage is less clear. Prophylactic treatment for the prevention of the first haemorrhage from oesophageal varices (pharmacological, but also endoscopic or surgical) is justified only in strictly selected patients with a high risk of haemorrhage.
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PMID:[Pharmacotherapy of portal hypertension]. 776 77

Intracerebroventricular (i.c.v.) infusions of angiotensin II (AII) reliably induced c-fos expression in the supraoptic (SON) and paraventricular (PVN) nuclei, as well as other areas of the basal forebrain including the OVLT, subfornical organ (SFO), and bed nucleus (BNST). Double-labelling showed that AII-induced c-fos was observed in both vasopressin (AVP-) and oxytocin (OXY)-containing neurons of the SON and PVN in male rats. Allowing rats to drink water after AII infusions suppressed c-fos expression both AVP- and OXY-stained magnocellular neurons. Intragastric infusions of water were also effective, showing that oro-pharyngeal stimuli were not critical. Maximal suppression occurred in rats in whom water had been infused intragastrically about 5 min before i.c.v. AII infusions, suggesting that changes in osmolarity were responsible. i.c.v. AII also induced c-fos expression in a number of brainstem structures, including the solitary nucleus (NTS), lateral parabrachial nucleus (LPBN), locus coeruleus (LC), and the area postrema (AP). These results indicate that AVP and OXY-containing neurons in the magnocellular parts of the SON and PVN alter their immediate-early gene response to AII after water intake, and that this does not depend upon oro-pharyngeal factors. Furthermore, AII can induce c-fos expression in a number of brainstem nuclei associated with autonomic function, and these do not respond to water intake.
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PMID:Regional suppression by water intake of c-fos expression induced by intraventricular infusions of angiotensin II. 782 Jun 57

In 40 patients with esophageal varices, esophageal variceal pressure was assessed endoscopically using a pneumatic pressure sensor. The effects of vasopressin or nitroglycerin on variceal pressure and endoscopic findings were also assessed in two groups of seven patients. The results were as follows: (1) Variceal pressure was increased above 250 mmH2O in all patients who had bled, and the mean variceal pressure was significantly higher in patients who had bled than in those who had not (301 +/- 47 vs. 230 +/- 58 mmH2O respectively, p < 0.001). (2) Variceal pressure correlated with endoscopic findings, determined using the criteria of the Japanese Research Society for Portal Hypertension. It was significantly higher when varices with a feature of F2-F3 or RC(+2)-RC(+3) were compared to those with a feature of F1 or RC(-)-RC(+), respectively. (3) Both groups given vasopressin or nitroglycerin had significant reductions in variceal pressure; however, there was little improvement in endoscopic findings in those given nitroglycerin, compared to the improvement in those given vasopressin. Thus, use of a pneumatic pressure sensor proved to be a pertinent tool for assessing esophageal varices, along with endoscopic signs.
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PMID:Clinical significance of esophageal variceal pressure in patients with esophageal varices. 783

Between 1988 and 1990 an unblinded, randomized trial of terlipressin or vasopressin plus transdermal nitroglycerin, as part of a treatment strategy including emergency sclerotherapy for actively bleeding varices, was conducted during 165 admissions in 137 patients with cirrhosis and upper digestive bleeding. Eighty-four patient admissions were assigned to terlipressin (2 mg every 6 h) and 81 to vasopressin (0.4 to 0.8 unit per min) plus transdermal nitroglycerin (20 to 80 mg). The two groups were comparable for relevant clinical data, but there were slightly more patients with hepatocellular carcinoma or terminal conditions in the terlipressin group. After the 24-h study period, failure to control bleeding was 20/84 (25%) in the vasopressin and 14/81 (17%) in the terlipressin group (p = 0.19). Corresponding figures for patients bleeding from varices (emergency sclerotherapy in 43 and 45, respectively) were 13/55 (24%) and 5/56 (9%; p = 0.035), from other sources 5/16 (31%) and 2/15 (13%; p = 0.23), from undefined sources 2/10 (20%) and 7/13 (54%; p = 0.1). In a logistic multivariate regression model the odds ratio for terlipressin adjusted for prognostic factors was 0.45 (p = 0.07). There were seven major side effects requiring treatment discontinuation in the vasopressin and one in the terlipressin group. These results suggest that terlipressin alone is as effective as vasopressin plus transdermal nitroglycerin, with less severe side effects, in 24-h control of upper gastrointestinal bleeding in patients with cirrhosis.
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PMID:Terlipressin or vasopressin plus transdermal nitroglycerin in a treatment strategy for digestive bleeding in cirrhosis. A randomized clinical trial. Liver Study Group of V. Cervello Hospital. 800 1

Pharmacological management of acute variceal hemorrhage appears to be effective in patients with liver cirrhosis. Somatostatin and presumably its longer-acting analog, octreotide, are more efficient and safer than other vasoconstrictors like vasopressin, terlipressin or their combination with nitroglycerin. Drug treatment, however, usually represents only a valuable adjunct to other measures to stop bleeding such as endoscopic variceal sclerotherapy. Prophylaxis of first bleeding by beta-blockade appears justified in patients at a high risk of bleeding which still has to be defined more precisely. Prevention of recurrent hemorrhage can be effective in some but not in all of the patients with liver cirrhosis and a first bleeding episode. Treatment of patients with good liver function under direct control of the wedged hepatic vein pressure gradient presumably will reduce the failure rate of prophylaxis with beta-blockade.
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PMID:The role of drug treatment in variceal bleeding. 811 90


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