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 (Pitressin) infusion through peripheral veins is a commonly used modality for control of bleeding esophageal varices. In this report we describe the development of infected gangrene at the site of accidental vasopressin infiltration in a patient with diabetes mellitus, cirrhosis and bleeding esophageal varices. Among the explanations for the development of gangrene are: 1. continuous intravenous administration; 2. diabetic peripheral vascular disease; 3. mechanical compression of extravasated fluid in a closed space. No antagonist has been clinically proven to reverse the vasoconstrictive effects of vasopressin.
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PMID:Infected gangrene. A serious complication of peripheral vasopressin administration. 741 38

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

Numerous conditions lead to portal hypertension with the development of esophageal varices. Treatment for acute variceal hemorrhage should progress in a logical, stepwise fashion. Therapy after fluid resuscitation includes vasopressin, somatostatin, or a Sengstaken-Blakemore tube. This is followed by treatment with sclerotherapy, variceal ligation, or a combination of both. Continued bleeding is managed by more invasive measures that include radiologic embolization or shunting, esophageal transection, distal splenorenal shunt, or liver transplantation. Beta-blockade may be useful to prevent recurrent bleeding in compliant patients without medical conditions that would preclude use of beta-blockade. Once control of the bleeding has been achieved, sclerotherapy or ligation should be used to obliterate the varices, but prophylactic use of sclerosant is not particularly beneficial.
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PMID:Esophageal varices. 781 45

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

A prospective randomized trial was conducted in unselected, consecutive patients with bleeding esophageal varices resulting from cirrhosis comparing (1) emergency portacaval shunt performed within 8 hr of initial contact (21 patients) with (2) emergency medical therapy (intravenous vasopressin and esophageal balloon tamponade) followed in 9 to 30 days by elective portacaval shunt in survivors (22 patients). All patients underwent the same diagnostic workup within 3 to 6 hr of initial contact, and received identical supportive therapy initially. All patients were followed up for at least 10 yr. The protocol contained no escape or cross-over provisions. There were no statistically significant differences between the two treatment groups in the incidence of any of the clinical variables, results of laboratory tests or degree of portal hypertension. Child's risk classes in the shunt group were A-2 patients, B-8 patients and C-11 patients, whereas in the medical group they were A-10 patients, B-5 patients, and C-7 patients, a significant difference (p < 0.01) that might have favored emergency medical treatment. Bleeding was controlled initially and permanently by emergency shunt in every patient, but by medical therapy in only 45% (p < 0.001). Mean requirement for blood transfusion was 7.1 +/- 2.6 units in the shunt group and 21.4 +/- 2.6 units in the medical group (p < 0.001). Eighty-one percent of the patients in the shunt group were discharged alive compared with 45% in the medical group (p = 0.027). Five- and 10-yr observed survival rates were 67% and 57%, respectively, after emergency shunt compared with 18% and 18%, respectively, after the combination of emergency medical therapy and elective shunt (p < 0.01). These survival rates produced by emergency shunt performed within 8 hr of initial contact confirm the effectiveness of this procedure observed in our previous unrandomized studies.
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PMID:Prospective randomized trial of emergency portacaval shunt and emergency medical therapy in unselected cirrhotic patients with bleeding varices. 792 12

Bleeding esophageal varices are a life-threatening complication of portal hypertension. During the emergent phase, nurses have an important role in assessing the patient's response to volume replacement and in monitoring interventions to control hemorrhage. Complications contribute to the high mortality associated with variceal hemorrhage. Knowledge of the pharmacologic side effects of vasopressin and of the potential complications associated with endoscopic injection sclerotherapy and esophagogastric balloon tamponade is critical for successful nursing management of the adult with bleeding esophageal varices. The goal of long-term management is to prevent recurrent hemorrhage. This is accomplished by repeated injection sclerotherapy and strategies to reduce portal pressure. Patient education is focused on modification of behaviors that increase the risk for bleeding and on the early recognition of recurrent bleeding.
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PMID:The adult with bleeding esophageal varices. 844 92

The pressure of oesophageal varices was determined by fine needle direct puncture in 19 patients with hepatitis B surface antigen (HBsAg)-positive cirrhosis after the first episode of variceal bleeding before endoscopic sclerotherapy. Both the stability and reliability of the measurement of intravariceal pressure by fine needle puncture were confirmed. Seven patients received intravenous 1 mL normal saline. Intravariceal pressure did not change before and after injection of normal saline (16.3 +/- 4.0 vs 16.0 +/- 4.0 mmHg, P > 0.05). Twelve patients received intravenous 1 units vasopressin and this caused a significant reduction in intravariceal pressure (15.6 +/- 2.6 vs 10.3 +/- 2.9 mmHg, P < 0.0001). The average basal intravariceal pressure in these patients was 15.8 +/- 3.1 mmHg. After intravariceal pressure was recorded, the needle was left in situ and endoscopic sclerotherapy commenced immediately. During the investigation, no adverse reaction or complication was encountered. It was concluded that the measurement of intravariceal pressure by fine needle direct puncture followed by immediate sclerotherapy is a safe and simple method to evaluate the short-term effect of drug prevention from oesophageal variceal bleeding and that vasopressin causes reduction of intravariceal pressure.
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PMID:Measurement of intravariceal pressure by fine needle direct puncture in hepatitis B surface antigen-positive cirrhotic patients: the effect of vasopressin. 847 53

Variceal hemorrhage is a leading cause of death in patients with hepatic cirrhosis. We report the case of two cirrhotic patients with hepatocarcinoma in whom oesophageal varices bled repeatedly. Because the bleeding was not controlled by sclerotherapy, vasopressin or Blakemore balloon, the patients were evaluated for emergency transjugular intrahepatic portosystemic shunt. After the procedure, portal vein pressure decreased from 45.5 mmHg to 18 mmHg and from 44 mmHg to 19 mmHg respectively and no filling of varices was evident at venogram or endoscopy. After 16 and 8 months respectively, bleeding had not recurred, and no episodes of encephalopathy were referred. Transjugular intrahepatic portosystemic shunt should always be considered an effective emergency therapeutic alternative to shunt surgery in patients with active variceal bleeding when traditional management fails.
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PMID:Emergency transjugular intrahepatic portosystemic shunt in patients with active variceal bleeding and hepatocarcinoma. 856 97

We present three patients with ornipressin-induced bradycardia, one of which developed also ventricular tachycardia of the torsade de pointes type. All three patients were treated with this vasopressin derivative because of bleeding esophageal varices due to portal hypertension in liver cirrhosis. Bradycardia ceased after discontinuing ornipressin therapy. One patient was treated successfully with atropine, one with isoprenalin and magnesium (he had to be defibrillated); the third patient recovered after cessation of ornipressin administration. Bradycardia is a known but rarely reported side effect of vasopressin and its derivatives. Animal studies suggest that this effect is due to its cardiodepressive action and also to a vagus-mediated reflex following vasopressin-induced increase in blood pressure. When injected directly into the ventricles of the brain, vesopressin leads to a decrease of the heart rate without affecting blood pressure; however, it remains unclear whether this mechanism is responsible for bradycardia after intravenous administration. Careful monitoring is essential during the treatment with vasopressin and its derivatives.
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PMID:[Clinico-pharmacological case (2). Bradycardia and ventricular tachycardia of the torsades de pointes type as a side effect of vasopressin: 3 case reports]. 864 94


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