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)

Oesophageal varices are found in the submucosa of the lower oesophageal sphincter (L.E.S.). Portagraphic studies after vasopressin administration showed occlusion of submucosal oesophageal varices and distension of the para-oesophageal veins. Oesophagography and endoscopy after administration of anticholinergics showed considerable dilatation of the submucosal oesophageal varices. Because vasopressin increases, and anticholinergics decrease, L.E.S. pressure it is suggested that L.E.S. pressure is an important factor in the development of submucosal oesophageal varices.
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PMID:How the lower oesophageal sphincter affects submucosal oesophageal varices. 8 85

Seven patients with compensated liver cirrhosis and esophageal varices, all with a base line wedge hepatic vein pressure greater than 20 cm H2O, received 1-mg doses of vasopressin hormonogen (tGLVP) intravenously. There was a significant mean decrease in wedge pressure of 32%, which lasted for at least 20 min (the duration of measurement), with no change in cardiac output measured. The only cardiac response was a 10 to 20% bradycardia at the height of the moderate pressor response-otherwise the ECG was without change. In 5 patients who received the same tGLVP dose during surgery, direct measurements of portal venous pressure showed the same degree of decrease within 10 min of intravenous injection. Fifteen patients with liver cirrhosis and severe bleeding from esophageal varices were treated conservatively with blood transfusion and tGLVP as the only major drug aside from antibiotics. A nonrandomized control group of 13 patients with the same age distribution, stage of disease, number of previous bleeds, etc., was treated conservatively in the same manner, except that they received either no hemodynamically active drugs or short acting neurohypophysial peptide preparations such as Pitressin. In the control group there was a 61.5% total mortality, a 53.8% mortality directly related to uncontrollable bleeding, and a mean duration of the bleeding episode of 11 days. In the tGLVP-treated group total mortality was 20%, mortality directly related to uncontrollable bleeding was 13.3%, and mean duration of the bleeding episode was 2.9 days. These results appear to justify a large scale clinical trial of the vasopressin hormonogen in this disease.
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PMID:Action of the triglycyl hormonogen of vasopressin (glypressin) in patients with liver cirrhosis and bleeding esophageal varices. 30 62

The results of surgical treatment of bleeding esophageal varices over an 8-year period in 155 patients are reviewed. Primary treatment of bleeding was conservative, with intravenous administration of vasopressin and balloon tamponade. Emergency operations were carried out after 48 hours in persons with persistent bleeding who were surgical candidates. Operative mortality was higher in this group (40%) than in those undergoing elective or urgent operations (each 10%). Postoperative encephalopathy occurred in 35% of patients and was correlated closely to late death after establishment of a shunt. The mesocaval shunt is no better than the portacaval but appears to be a good alternative in an emergency. In a controlled trial the distal splenorenal shunt was found to be associated with a lower rate of postoperative encephalopathy than the portacaval shunt, but thus far the long-term survival rates have not differed.
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PMID:Selection of operation in patients with bleeding esophageal varices. 30 80

Two patients developed local gangrene after subcutaneous infiltration of vasopressin (Pitressin, Parke, Davis & Company, Detroit, Mich.) utilized for the control of bleeding from esophageal varices. In the 1st patient, ischemic gangrene resulted in transmetatarsal amputation and also necessitated skin grafts on the forearm. The 2nd patient developed gangrene and clostridial sepsis and expired. The effects of systemically administered Pitressin are reviewed and suggestion to prevent local necrosis are presented.
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PMID:Local gangrene: a complication of peripheral Pitressin therapy for bleeding esophageal varices. 30 80

Lower gastrointestinal bleeding from intestinal varices cannot readily be detected at operation; hence, preoperative identification is important. Our experience with six patients having sudden, massive bleeding per rectum from intestinal varices suggests a group of common findings. These patients had cirrhosis, no blood in the stomach or duodenum, characteristic mucosal imprints on barium enema, or direct visualization of varices on sigmoidscopy or colonoscopy. Only two had demonstrable esophageal varices. The diagnosis was confirmed and the site of the varices localized on the venous phase of selective mesenteric angiography in five patients. Varices were located in the duodenojejunum in two, in the cecum and ascending colon in two, and in the rectum and sigmoid colon in two patients. Three patients were treated nonoperatively with transfusion and intraarterial infusion of vasopressin into the superior mesenteric artery; one died. One patient with cecal varices had a right hemicolectomy that controlled the bleeding, but progressive hepatic failure resulted in postoperative death. The remaining two patients had successful decompression of left colonic varices by portasystemic shunt.
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PMID:Massive lower gastrointestinal bleeding from intestinal varices. 31 92

The effect of vasopressin on the blood flow through experimentally induced esophageal varices and on the musculature of the lower end of the esophagus has been studied. The blood flow was measured by 85Kr injection into the portal vein and selective recording of the radioactivity of the blood flow through the varices. Simultaneous portography and recording of the portal and arterial blood pressure were performed. Following i.v. administration of vasopressin, there was seen a decrease in portal pressure and transient increase in arterial blood pressure. Simultaneously there was observed a decrease in blood flow through the varices, which were no longer visible at portography, while intra-esophageal pressure was increased. It is concluded that there is a dual mechanism of the effect of vasopressin on bleeding from esophageal varices. It reduces the portal pressure and it contracts the esophageal musculature with resultant compression of the afferent radicles to the submucosal esophageal varices.
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PMID:The mechanism of lysine-vasopressin hemostasis in bleeding esophageal varices. 31 46

For the initial control of haemorrhage from oesophageal varices, two methods of vasopressin administration have been compared--the conventional bolus of 20 units and a low dose infusion of 0.4 units per minute. Twenty patients bleeding from oesophageal varices, confirmed by endoscopy, were allocated into either treatment group (10 in each). Vasopressin infusion stopped bleeding in 86 per cent of the episodes in contrast to 12.5 per cent (P less than 0.01) with bolus doses. Balloon tamponade with a Sengstaken-Blakemore tube was used to control bleeding in only 2 episodes in patients on infusion and in 10 episodes in patients on bolus doses of vasopressin (P less than 0.05). Our study confirms that low dose vasopressin infusion in more effective in controlling bleeding from oesophageal varices than conventional bolus doses.
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PMID:Emergency treatment of variceal haemorrhage. 31 46

The percutaneous transhepatic portal vein catheterization (PTP) with selective obliteration of the coronary vein and/or the short gastric veins in treating bleeding esophageal varices was introduced in 1974. In order to prevent recanalization of the vessels Bucrylate (isobutyl-2-cyano-acrylate) has been used in 43 patients 55 times during a period of 34 months (October 1975 to July 1978). The obliterative treatment was followed by rebleeding in 35% of the cases and continued bleeding occurred in two patients. Fourteen patients were treated on 16 occasions during acute bleedings, and five of these (36%) died within two months from a portal vein thrombosis caused by the obliterative procedure. Because of these findings PTP with obliteration of the veins feeding the esophageal varices is not recommended as an elective way of treatment. It should only be used in the acute bleeding patient when transesophageal sclerosering therapy, continuous vasopressin infusion and balloon tamponade have failed. Fifty-six per cent of the patients acutely treated stopped bleeding for more than one week, thus avoiding an emergency shunt or devascularization operation which are associated with a high mortality rate.
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PMID:Obliteration of esophageal varices by PTP: a follow-up of 43 patients. 38 46

The cirrhotic patient with acute bleeding from esophageal varices has less than a 50% chance of leaving the hospital alive; the outlook for survival is so poor that even desperate measures are worthwhile. Some traditional nonsurgical methods for the control of the bleeding are either ineffective at worst or temporary at best. Balloon tamponade is not recommended at all, but intravenously administered vasopressin may be helpful in allowing the necessary diagnostic investigations to be completed. Most important at this stage are the measures necessary to improve the general status of the patient--restoration of blood volume with fresh blood, prevention of ammonia intoxication, support of the liver, correction of metabolic alkalosis and treatment of the hyperdynamic state with digitalis and cardiotonic drugs. Controlling the bleeding is not the greatest problem--the greatest problem is achieving survival of a critically ill patient who undergoes a formidable operation (e.g., variceal ligation stops the bleeding, but is itself an operation of considerable magnitude). In our hands emergency shunting is the best treatment providing a definitive procedure with the highest 10-year survival rate and the lowest complication rate.
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PMID:Emergency treatment of variceal hemorrhage. 38 92

In eight patients with cirrhosis of the liver and portal hypertension an intravenous infusion of lysine vasopressin induced a rapid increase in the plasma level of the fibrinolytic proenzyme plasminogen activator. In contrast, triglycyl lysine vasopressin (glypressin; GVP), in a dose known to lower portal venous pressure, produced no fibrinolytic response. This lack of fibrinolytic response represents an advantage of GVP over lysine vasopressin in addition to its longer in vivo half-life and lower cardiotoxicity. Clinical trials of GVP in the treatment of bleeding oesophageal varices are needed.
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PMID:Effects of lysine vasopressin and glypressin on the fibrinolytic system in cirrhosis. 48 51


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