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)

The author's current angiographic approach to the diagnosis and therapy of acute gastrointestinal (GI) bleeding is summarized and discussed. It is based on the authors' experience with diagnostic studies in more than 300 acute GI bleeders and the use of various angiotherapeutic techniques in 138 of them as well as the experience of others. A "moderately aggressive angiographic approach" is advocated for the diagnosis of acute GI bleeding in most patients with angiography used as needed after emergency endoscopy and preliminary medical therapy. Vasoconstrictive angiotherapy with selective intraarterial use of vasopressin is partially giving way to low dose, intravenous infusion of vasopressin and, where possible, to direct vascular occlusion. Selective transcatheter embolic occlusion of bleeding vessels is in indicated cases an accepted method for controlling arterial bleeding. Medical gelatin (Gelfoam) is the current authors' embolization material of choice. Selective variceal occlusion offers promising means for management of bleeding from gastroesophageal varices. Its possible combination with transcatheter intrahepatic portosystemic shunting might also provide non-surgical relief of portal hypertension.
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PMID:Current angiographic approach to diagnosis and therapy of acute gastrointestinal bleeding. 13 92

Twenty patients with massive abdominal hemorrhage related to chronic pancreatitis, pancreatic neoplasms and arteriovenous malformations were studied angiographically. Abdominal hemorrhage drained most frequently into the gastrointestinal tract, but also flowed through cutaneous drain sites and fistulas, intraperitoneally, into pseudocysts and once into a large pancreatic tumor. The most common angiographic observation in pancreatitis was pseudoaneurysm formation. Both patients with arteriovenous malformation had dilated, racemose feeding arteries and early dense filling of the draining veins. Three patients had pancreatic carcinoma and documented bleeding from gastroesophageal varices related to portal or splenic vein occlusion by the tumor. Five patients were treated by vasopressin infusion, balloon tamponade, or therapeutic embolization.
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PMID:Angiography of massive hemorrhage secondary to pancreatic diseases. 30 42

From July 1975 to November 1976 25 patients with bleeding esophagogastric varices documented by endoscopy who failed to respond to conservative medical treatment were transferred to the Surgical Service. These patients, who were mainly Child's Class "C" alcoholic cirrhotic patients, were treated with vasopressin infused continuously using a standardized dose into either a peripheral vein or the superior mesenteric artery (SMA) according to a predetermined randomization. No significant difference in efficacy for control of bleeding (average rate = 56%) related to route of administration was found. Because catheter-related complications in the SMA group were significantly greater, we concluded that the method of choice in vasopressin treatment of esophagogastric variceal bleeding is a continuous infusion by way of a peripheral vein.
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PMID:Control of bleeding varices by vasopressin: a prospective randomized study. 30 11

The effect of vasopressin on the lower esophageal sphincter has been investigated in 12 healthy volunteers. Peripheral infusion of 0.2 U/min resulted in a significant (p less than 0.05) decrease in sphincter pressure. Accordingly, vasopressin-induced myogenic compression of bleeding varices has been ruled out as a potential additional hemostatic mechanism of vasopressin.
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PMID:[Effect of vasopressin on the lower esophageal sphincter. Study on the action mechanism of vasopressin in bleeding esophageal varices]. 30 14

The angiographic technique percutaneous transhepatic coronary vein occlusion was used to treat esophagogastric variceal bleeding in 38 patients. There were two categories of patients: those actively bleeding who had not been controlled by continuous vasopressin infusion and/or Blakemore tube tamponade, and those with portal hypertension who were not actively bleeding at the time of transhepatic portal venography but who were at high risk for recurrent variceal hemorrhage. Coronary vein occlusion was achieved in 33 patients by (1) metal clip and cotton devices(one); (2) balloon catheter occlusion (two); (3) heat-treated autogenous clot and powdered absorbable gelatin sponge (Gelfoam) (13); and (4) Gelfoam strips soaked in sodium tetradecyl sulfate (17). Percutaneous coronary vein occlusion was effective in controlling 81% of the patients with actively bleeding varices. In patients who were not actively bleeding, percutaneous transhepatic coronary vein occlusion seemed to afford good protection for recurrent variceal hemorrhage.
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PMID:Esophagogastric variceal hemorrhage: its treatment by percutaneous transephatic coronary vein occlusion. 30 25

Infusions of intraarterial vasopressin (IAV) into the superior mesenteric artery have been shown to be effective in controlling hemorrhage from esophagogastric varices. Intravenous infusions of vasopressin (IVV), which can be initiated rapidly and require less sophisticated equipment and personnel, have also been reported to control variceal hemorrhage. We undertook a controlled clinical trial to compare these two routes of administration. Twenty-two cirrhotic patients with massive hemorrhage from varices were randomized to receive either IVV or IAV. Intraarterial vasopressin was begun at 0.1 U/min and increased progressively as needed to 0.2, 0.3, 0.4, and 0.5 U/min. Intravenous vasopressin was begun at 0.3 U/min and increased progressively as needed to 0.6, 0.9, 1.2, and 1.5 U/min. Hemorrhage was controlled in 5 of 10 episodes (50%) with IVV and in 6 of 12 episodes (50%) with IAV. Seven of the ten episodes treated with IVV (70%) ended fatally compared with 9 of 12 treated with IAV (75%). Side-effects and complications occurred with similar frequency in the two groups. The two routes of administration are equal in effects, side-effects, and complications. We recommend that IVV, which can be administered more easily, be given a brief therapeutic trial early in the management of hemorrhage from varices.
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PMID:A controlled comparison of continuous intraarterial and intravenous infusions of vasopressin in hemorrhage from esophageal varices. 31 53

Percutaneous transhepatic portal venography is a relatively safe method of obtaining both physiologic and morphologic information in patients with portal hypertension. Precise "road mapping" is performed, as well as measurement of free portal pressure. Additionally, transcatheter obliteration of gastroesophageal varices may produce effective cessation of hemorrhage in patients bleeding from this site, as was done on an emergency basis after failure of intra-arterial vasopressin infusion.
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PMID:Percutaneous transhepatic portal venography in the diagnosis and management of gastroesophageal varices. 31 59

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

The presence of mesenteric varices was demonstrated angiographically in 7 patients with portal hypertension. In 4 of these cases the mesenteric varices were the source of lower gastrointestinal bleeding which was successfully controlled by intra-arterial infusion of vasopressin. The radiological diagnosis and management of mesenteric varices is discussed and the pertinent literature is briefly reviewed.
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PMID:Mesenteric varices: a source of mesosystemic shunts and gastrointestinal hemorrhage. 31 1


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