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)

Two patients with severe liver disease developed scrotal necrosis after intravenous vasopressin infusion for bleeding esophageal varices. One of these patients also developed anterior abdominal wall skin necrosis. Although ischemic complications secondary to vasopressin are probably not totally avoidable, attention to hypovolemia, concomitantly administered pressor drugs, patient position, and points of local pressure may decrease the likelihood of these previously unreported complications.
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PMID:Scrotal and abdominal skin necrosis complicating intravenous vasopressin therapy for bleeding esophageal varices. 315 56

Due to the marked effects of hemorrhage on cardiac output and splanchnic hemodynamics, the circulatory actions of vasopressin may differ during bleeding as opposed to stable conditions. We evaluated this hypothesis in conscious rats with portal hypertension due to chronic portal vein stenosis, by comparing the effects of a vasopressin infusion (0.02 IU per kg per min) to those of a control saline infusion, during and after a hypotensive hemorrhage (25 ml per kg). We also studied unbled portal hypertensive rats receiving an identical infusion of vasopressin or saline. During and after hemorrhage, vasopressin induced significant changes in systemic hemodynamics but had no effect on portal pressure, portal tributary blood flow and nonhepatic splanchnic arteriolar resistance. In unbled animals, by contrast, vasopressin decreased portal pressure and portal tributary blood flow and increased nonhepatic splanchnic arteriolar resistance. Our data further indicate that hemorrhage alone caused an early vasoconstriction in the portal tributaries and a delayed vasoconstriction in the nonsplanchnic vascular bed while vasopressin during hemorrhage induced an early and sustained vasoconstriction in the nonsplanchnic vascular bed as well as in the portal tributaries. The results show that, during and after severe bleeding, vasopressin exerts little influence on portal hemodynamics. Although these data do not allow firm conclusions concerning the therapeutic efficacy of vasopressin in bleeding esophageal varices, they demonstrate that the splanchnic actions of vasoactive substances cannot be readily extrapolated from stable conditions to hemorrhage.
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PMID:Lack of vasopressin action on splanchnic hemodynamics during bleeding: a study in conscious, portal hypertensive rats. 325 54

Based on laboratory and clinical data from our institution, 113 patients with cirrhosis, portal hypertension, and acute hemorrhage from esophageal varices were treated with high-dose vasopressin arginine (1 to 1.5 U/min) to control the acute bleeding and reduce blood loss during portosystemic shunt operations. Compared with patients receiving a lower dose of vasopressin infusion, these patients had a reduction in both postoperative mortality (21% vs 6%) and the proportion of patients requiring emergency operation (40% vs 18%). A decrease in operative blood loss (1340 vs 793 mL) was also seen. Adverse effects of vasopressin were increased by high-dose infusion, but no significant morbidity occurred. These results suggest that high-dose vasopressin infusion can reduce the mortality of acute variceal hemorrhage and porto-systemic shunting primarily by allowing patients to improve hepatic function prior to an elective operation and by decreasing intraoperative blood loss.
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PMID:High-dose vasopressin for acute variceal hemorrhage. Clinical advantages without adverse effects. 326 96

Endoscopic injection sclerotherapy of oesophageal varices was performed in 71 patients: 50 with intrahepatic and 21 with extrahepatic block. In summary 330 procedures were done: 220 under general anaesthesia using the Negus rigid oesophagoscope and 110 with diazepam as premedication using a flexible, fibreoptic endoscope. Definitive control of variceal haemorrhage was achieved in 30 of 34 emergency admissions (88%). The hospital mortality in acute variceal bleeding was 26.5%. Elective, repeated sclerotherapy was performed in 60 patients. In 43 patients complete obliteration of varices or their marked reduction were observed. Rebleeding occurred in 23% and major complications in 17% of patients. The overall one year survival rate was 82%. We consider sclerotherapy as a method of choice in bleeding oesophageal varices uncontrollable by vasopressin and balloon tamponade. It also represents a valuable method of preventing rebleeding particularly in patients with a high operative risk.
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PMID:Emergency and elective sclerotherapy of oesophageal varices. 326 65

Endoscopic reflectance spectrophotometry was used to compare the effect of vasopressin and propranolol on gastric mucosal hemodynamics in dogs with surgically induced esophageal varices and prehepatic portal hypertension. Reflectance spectrophotometry provides indices of mucosal hemoglobin concentration (IHB) and oxygen saturation (ISO2). Hyperemia (increased IHB, normal ISO2), ischemia without congestion (decreased IHB, decreased ISO2), and ischemia with congestion (increased IHB, decreased ISO2) are accompanied by characteristic patterns of IHB and ISO2. Under anesthesia, measurements were obtained on separate days from the gastric corpus mucosa of eight dogs before and 2 to 10 min after either 1 to 5 units of intravenous vasopressin or 1 mg of propranolol. Results revealed that vasopressin (in doses that significantly reduced variceal and portal venous pressure in this animal model) produced a reduction in both IHB and ISO2, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. On the other hand, propranolol in a dose that significantly reduced pulse rate by 27 +/- 2% had no effect on IHB or ISO2, suggesting that this dose of propranolol has no direct vasoactive effect on the gastric (splanchnic) circulation.
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PMID:Endoscopic demonstration that vasopressin but not propranolol produces gastric mucosal ischemia in dogs with portal hypertension. 326 2

A patient had bilateral tympanic membrane rupture and otorrhagia, an unusual complication of continuous positive airway pressure (CPAP). CPAP, applied by a bag/mask system using disposable spring valves, was used to treat acute pulmonary edema during volume resuscitation and vasopressin therapy for bleeding from esophageal varices.
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PMID:Bilateral otorrhagia associated with continuous positive airway pressure. 328 Feb 64

The present study investigated to what extent measurements of wedged and free hepatic venous pressures adequately reflect the effects of vasopressin at the esophageal varices in patients with cirrhosis. Eleven patients undergoing therapeutic sclerotherapy were studied by measuring wedged hepatic venous pressure, intravariceal pressure, free hepatic venous pressure, superior vena cava pressure and the intravascular pressure gradients wedged hepatic venous pressure-free hepatic venous pressure and intravariceal pressure-superior vena cava pressure, prior to and after vasopressin injection (1 IU, iv). Vasopressin caused a significant reduction in intravariceal pressure (from 22.5 +/- 9.4 to 19.2 +/- 8.4 mm Hg, p less than 0.001). Measurement of wedged hepatic venous pressure and free hepatic venous pressure closely reflected the reduction in variceal pressure. Thus, wedged hepatic venous pressure decreased by 16 +/- 11%, which is close to the 14 +/- 7% change in intravariceal pressure, and the 23 +/- 12% fall in the pressure gradient wedged hepatic venous pressure-free hepatic venous pressure was mirrored by the 26 +/- 10% change in intravariceal pressure-superior vena cava pressure. These pressure gradients decreased more than the absolute pressures (intravariceal pressure and wedged hepatic venous pressure) due to concomitant increases in superior vena cava pressure (1.9 +/- 1.9 mm Hg) and free hepatic venous pressure (0.6 +/- 1.9 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of vasopressin on the intravariceal pressure in patients with cirrhosis: comparison with the effects on portal pressure. 339 13

The authors report their experience with immediate endoscopic injection sclerosis at the time of diagnosis of active bleeding esophageal varices compared to delayed sclerotherapy performed after control of variceal bleeding with vasopressin and Sengstaken-Blakemore tamponade. Twenty-eight active index bleeders and 20 active rebleeders were treated by immediate endoscopic injection sclerosis, which could technically be performed on all of the former and in 18 of the rebleeders (96%). Immediate control of active bleeding was achieved in all patients whose varices were injected (100%). Control at 48 hours was 89% for the index bleeding group and 80% for the rebleeding group. In the delayed sclerotherapy group of 19 patients, initial control (79%) and 48-hour control (64%) were significantly less. The rebleeding rate, complications, and death from exsanguination were greater in the delayed group, whereas longevity was similar in both groups. We conclude that immediate sclerotherapy effectively controls acutely bleeding esophageal varices with a lower complication rate than sclerotherapy performed after conventional medical therapy with vasopressin and Sengstaken-Blakemore tube tamponade.
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PMID:A comparison of immediate versus delayed endoscopic injection sclerosis of bleeding esophageal varices. 349 5

We report the occurrence of acute portal vein thrombosis in three patients undergoing endoscopic variceal sclerosis (EVS) for bleeding esophageal varices. All patients received intravenous vasopressin in close proximity to or at the time of EVS. By increasing flow of sclerosant caudally into gastric veins during EVS, vasopressin may predispose to retrograde propagation of thrombus into the portal venous system. Combined use of vasopressin and EVS for treatment of bleeding esophageal varices should be undertaken with caution.
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PMID:Portal vein thrombosis following combined endoscopic variceal sclerosis and vasopressin therapy for bleeding varices. 350 Jun 37

The effect of terlipressin (N-alpha-triglycyl-8-lysine-vasopressin) in bleeding esophageal varices was evaluated in a prospective placebo-controlled study. Fifty bleeding episodes from esophageal varices in 34 patients were randomized. Standard therapy with transfusions, fluid and electrolyte correction, and lactulose was performed in both groups. Balloon tamponade was used in 20 bleeding episodes in the terlipressin group and in 19 bleeding episodes in the control group. In the terlipressin group, hemorrhage was controlled in all bleeding episodes (25/25) whereas in the placebo group, only 20 of 25 bleeding episodes could be stopped within 36 hr (p less than 0.05). Sclerotherapy was performed in five bleeding episodes in the terlipressin group and in seven bleeding episodes in the placebo group. Treatment failures, including patients who required sclerotherapy, occurred in five bleedings in the terlipressin group and in 12 in the control group (p less than 0.05). The hospital mortality rate was 12% (3/25) in the terlipressin group and 32% (8/25) in the control group. Patients in the terlipressin group required fewer transfusions, the balloon needed to be inflated for a shorter time and the duration of bleeding was shorter than in the control group. However, these differences were not significant. These data do not allow conclusions concerning monotherapy with terlipressin, but they indicate that the addition of terlipressin to standard therapy may increase the control rate in acute variceal hemorrhage.
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PMID:Terlipressin in bleeding esophageal varices: a placebo-controlled, double-blind study. 351 Sep 47


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