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)

Serum gastrin increased in patients with pernicious anaemia after a beef-meal, but decreased after an oral load of glucose, xylose or sodium chloride. 50 g of glucose and 25 or 75 g of xylose suppressed serum gastrin to approximately 40% of basal values at 60 min and were slightly more effective than 10 g of sodium chloride. There was no rise in beef-meal stimulated serum gastrin concentration in vagotomized patients and only a slight rise in two patients with duodenal ulcer when an oral dose of 10 g of sodium chloride was given together with the beef-meal. 25 g of xylose suppressed basal serum gastrin concentration significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in six vagotomized patients. Nasal administration of small amounts of vasopressin decreased basal serum gastrin significantly in all subjects examined. Further studies indicated, however, that vasopressin was only effective when pharmacological plasma concenten orally and intraduodenally were compared in six patients with pernicious anaemia. Serum gastrin concentration decreased approximately to the same extent in both experiments. It is concluded that the inhibitory effect of glucose on gastrin secretion most likely is mediated hormonally via osmo-receptors located in the small intestine.
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PMID:Inhibition of gastrin secretion by hypertonic solutions in patients with pernicious anaemia and duodenal ulcer. 11 45

This study was undertaken to ascertain whether the modern effective anti-ulcer drugs have had any influence on the natural history of hemorrhagic peptic ulcer disease and other acid-related gastroduodenal bleeding disorders. In the prospective part of the study the anamnestic data of all 73 patients admitted to our hospital with a bleeding ulcer or related disease during the year 1989 were compared with the data of 73 patients subjected to elective upper GI tract endoscopy for abdominal symptoms other than bleeding, paying special attention to potential risk factors. There were no differences in previous ulcer history or operations for ulcer disease between these two groups. Cigarette smoking and coffee consumption were not different, but the bleeders consumed alcohol more often, and, in particular, they used ulcerogenic drugs or other hemorrhagic diathesis-provoking agents significantly more frequently than controls. In the retrospective part of the study these 73 patients were compared with the medical records of all 87 patients admitted to our hospital in 1976 for a bleeding peptic ulcer disease, to ascertain whether introduction of H2-blocking agents had had any influence on the nature of the patient population, characteristics of the disease, and severity of bleeding. The patients had become slightly older, and male preponderance was seen in both groups. The proportion of gastric ulcer had decreased, and duodenal ulcer had increased. In general, the bleeding seemed to become less severe but was more severe among women in both groups. In 1989 almost all patients were treated with H2 antagonists, and seven patients received additional medical therapy (vasopressin, somatostatin, or tranexamic acid).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peptic ulcer bleeding today: risk factors and characteristics of the disease. 168 92

Combining careful medical preparation with subsequent selective intravascular sclerotherapy, one-year survival rate of patients with bleeding oesophageal varices was increased to 90%. Of 41 patients with bleeding oesophageal varices, class Child A-C, none died of bleeding from the varices within the first year after sclerotherapy. Four patients died within the first year, two from liver failure due to severe alcohol abuse, one from liver failure with terminal primary biliary cirrhosis and one from an undiagnosed bleeding duodenal ulcer. Improved results were obtained by two measures: (1) instead of immediate sclerosing at time of diagnosis, initial arrest of bleeding with a Sengstaken tube and, if necessary, administration of vasopressin and improvement in general status by intensive measures to stabilise the circulation and clotting mechanism; (2) selective radiologically controlled intravascular sclerotherapy with a flexible special endoscope 1-2 days after admission. The particular advantage of selective intravascular sclerosing, though it is complicated, lies in the fact that fundal varices and supplying veins to the stomach can also be sclerosed and severe early as well as late complications are exceedingly rare.
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PMID:[Treatment of bleeding oesophageal varices. Results of combined medical and endoscopically selective intravascular sclerotherapy]. 698 6

Peptic ulcer is a common disorder of gastrointestinal system and its pathogenesis is multifactorial, where smoking and nicotine have significant adverse effects. Smoking and chronic nicotine treatment stimulate basal acid output which is more pronounced in the smokers having duodenal ulcer. This increased gastric acid secretion is mediated through the stimulation of H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking also increases bile salt reflux rate and gastric bile salt concentration thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, nonsteroidal anti-inflammatory drugs or cold restrain stress. Polymorphonuclear neutrophils (PMN) play an important role in ulcerogenesis through oxidative damage of the mucosa by increasing the generation of reactive oxygen intermediates (ROI), which is potentiated by nicotine and smoking. Nicotine by a cAMP-protein kinase A signaling system elevates the endogenous vasopressin level, which plays an aggressive role in the development of gastroduodenal lesions. Smoking increases production of platelet activating factor (PAF) and endothelin, which are potent gastric ulcerogens. Cigarette smoking and nicotine reduce the level of circulating epidermal growth factor (EGF) and decrease the secretion of EGF from the salivary gland, which are necessary for gastric mucosal cell renewal. Nicotine also decreases prostaglandin generation in the gastric mucosa of smokers, thereby making the mucosa susceptible to ulceration. ROI generation and ROI-mediated gastric mucosal cell apoptosis are also considered to be important mechanism for aggravation of ulcer by cigarette smoke or nicotine. Both smoking and nicotine reduce angiogenesis in the gastric mucosa through inhibition of nitric oxide synthesis thereby arresting cell renewal process. Smoking or smoke extract impairs both spontaneous and drug-induced healing of ulcer. Smoke extract also inhibits gastric mucosal cell proliferation by reducing ornithine decarboxylase activity, which synthesises growth-promoting polyamines. It is concluded that gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
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PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84

The use of reflectance spectrophotometry (RS) for mucosal hemodynamic measurement relies on the recognition of changes in indexes of mucosal hemoglobin concentration and oxygen saturation. Endoscopic application in clinical studies has confirmed important observations demonstrated in animal experiments. The vasoconstriction induced by propranolol, vasopressin, glypressin, or somatostatin in the portal hypertensive gastric mucosa and the reduction of gastroduodenal mucosal perfusion by nonsteroidal anti-inflammatory drugs (NSAIDs) or smoking, mesenteric venoconstriction associated with systemic hypoxia, and acid-induced duodenal hyperemia are important examples. Prognostic predictions include the development of stress-induced gastric ulcerations in patients with significant reductions in gastric perfusion after thermal or head injury, or the demonstration of delayed gastric or duodenal ulcer healing when the hyperemia at the ulcer margin fails to materialize. In mechanical-ventilator-dependent patients with sepsis, a significantly reduced gastric mucosal RS measurement portends a grave prognosis (mortality >80%). Recent advances in technology resulted in the construction and validation of instruments for visible light spectroscopy. Measurements focused on tissue oxygen saturation demonstrated epinephrine and vessel-ligation-induced vasoconstriction, the absence of ischemia in radiation-induced rectal telangiectasias, and gut ischemia responsive to revascularization treatment. Endoscopic RS and visible light spectroscopy are suitable for assessing the role of blood flow in conditions with a lesser degree of ischemia and for testing the hypothesis that functional dyspepsia and dysmotility syndromes may be due to gut ischemia.
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PMID:Endoscopic reflectance spectrophotometry and visible light spectroscopy in clinical gastrointestinal studies. 1793 61