Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors review the role of the gastroduodenal blood flow as a factor ensuring the secretory activity and protective properties of the gastric mucosa. The possibilities of its pharmacoregulation are also reviewed. It has been shown that the decrease of the gastric blood flow in experimental hemorrhagic shock, extravasal celiac artery stenosis, effects of indomethacin, vasopressin, etc. leads to ischemic injuries to the gastric mucosa accompanied by serious morphological and functional disturbances. The pathogenetic aspects of ischemic injuries to the stomach and duodenum are confirmed by the results of clinical examinations of patients with compression celiac artery stenosis and peptic ulcer. It has been noted that in these patients, the tissue blood flow in the mucosa in considerably decreased in the area of ulcerous defect. The lowering of the content of total phospholipids and changes in their composition were also observed both in relapse and after healing. Out of agents that improve peripheral circulation, propranolol, tavegil combined with cimetidine, trimin appeared most potent. These drugs regulate metabolic processes in gastric tissue, normalizing blood flow, reducing the content of histamine, serotonin, lipid peroxidation products, raising the level of total phospholipids and pepsin.
 ...
PMID:[Physiological significance of gastroduodenal blood flow and possibilities of its regulation by drugs]. 128 20

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)
 ...
PMID:Peptic ulcer bleeding today: risk factors and characteristics of the disease. 168 92

Plasma atrial natriuretic factor, aldosterone, renin activity, and antidiuretic hormone were studied in low output heart failure syndromes: cardiogenic shock in ten patients with acute myocardial infarction of the anterior wall (first group), hypovolemic shock after melena from peptic ulcer in ten subjects (second group), and hypotension with bradycardia syndrome in ten patients with acute myocardial infarction of the inferior wall (third group). Circulating atrial natriuretic factor in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) was significantly higher than in healthy volunteers matched for sex and age (8.4 +/- 0.3 pg/ml). In these patients there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the second and third groups were within normal range. Plasma aldosterone was high in all groups, plasma renin activity was elevated in the first and third groups, and high antidiuretic hormone was observed in the first and second groups. These findings indicate that in low output heart failure syndromes only hemodynamic changes affecting the atria stimulate atrial natriuretic factor release. No correlations were found between plasma atrial natriuretic factor and other hormones. In particular, high atrial natriuretic factor levels in the patients with cardiogenic shock did not inhibit release of aldosterone, renin, or antidiuretic hormone. It may be surmised that in these patients the hemodynamic effects override the inhibitory effects of atrial natriuretic factor.
 ...
PMID:Plasma atrial natriuretic factor in low output heart failure syndromes. 213 7

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Atrial natriuretic factor in cardiogenic shock, in hypovolemic shock and in the bradycardia-hypotension syndrome following acute myocardial infarction]. 253 Jan 27

Intravenous (IV) vasopressin has been used to control human upper gastrointestinal (GI) hemorrhage for over 30 years. Although the use of vasopressin has been studied extensively in adults, no study has evaluated its use in children. Vasopressin was used therapeutically in 15 episodes of esophageal variceal hemorrhage and two episodes of bleeding peptic ulcer. Nine of 17 episodes were controlled with vasopressin alone (53%). Balloon tamponade and variceal sclerosis were required for control in the remainder. Blood requirements averaged 53 mL/kg prior to control of hemorrhage. Metabolic complications occurred in 65% of the episodes. There were two groups of patients identified: those receiving greater or those receiving less than .01 units/kg/min of IV vasopressin. All of the complications identified occurred when greater than .01 U/kg/min of vasopressin were used (P less than .05). Control of bleeding was not improved with higher doses of vasopressin. These data suggest that the use of IV vasopressin at doses greater than .01 U/kg/min to control GI bleeding will increase the incidence of complications without improving control of hemorrhage.
 ...
PMID:Intravenous vasopressin and gastrointestinal hemorrhage in children. 314 93

The effect of somatostatin on splanchnic hemodynamics was determined in 8 patients with cirrhosis of the liver and in 18 normal subjects using arterial-hepatic-venous catheterization. Estimated hepatic blood flow determined by indocyanine green infusion was 1.36 +/- 0.23 L/min (+/- SEM) in patients with cirrhosis and remained unaffected during 30 min of somatostatin (250 microgram/h) administration. Wedged hepatic venous pressure which was elevated to 23 +/- 1.8 mmHg was also uninfluenced. In contrast to somatostatin, an infusion of vasopressin (12 U/h for 30 min) given to the same patients, lowered estimated blood flow by 28% (p < 0.05) and wedged hepatic venous pressure by 18% (p < 0.02). Arterial gastrin and insulin levels were lowered during somatostatin infusion by 33% (p < 0.02) and by 75% (p < 0.005), respectively. In contrast to the cirrhosis, infusion of 250 microgram/h somatostatin into normal subjects was associated with a decrease of estimated hepatic blood flow from 1.20 +/- 0.16 to 0.88 +/- 0.12 L/min (p < 0.01) representing a 27% decline. Arterial gastrin and insulin concentrations were lower (p < 0.01) than in cirrhosis, but the basal levels were lowered by somatostatin to a similar degree in both groups of patients. A higher dose of somatostatin (500 microgram/h) administered to normal subjects resulted in a similar decrease of gastrin and of estimated hepatic blood flow as that seen with 250 microgram/h, whereas a lower dose (125 microgram/h) decreased gastrin but failed to influence estimated hepatic blood flow. Thus, somatostatin at a dose which has been used in the treatment of acute peptic ulcer hemorrhage (250 microgram/h) failed to influence estimated hepatic blood flow and wegded hepatic venous pressure in patients with cirrhosis but lowered splanchnic blood flow in normal subjects. Assuming that this effect contributes to somatostatin's therapeutic efficacy, these results cast doubt on its potential value in the treatment of upper gastrointestinal bleeding of cirrhotics with portal hypertension.
 ...
PMID:Effect of somatostatin on splanchnic hemodynamics in patients with cirrhosis of the liver and in normal subjects. 610 98

The pathogenesis of peptic ulcer disease is multifactorial, including the effects of Helicobacter pylori, gastric acid, pepsin, gastroduodenal motility, smoking and nicotine, and the complex interaction of an array of other so-called aggressive and protective factors. Since the discovery and acceptance of H. pylori as a major etiologic agent in peptic ulcer disease, the role of smoking has received less attention. Smokers are more likely to develop ulcers, ulcers in smokers are more difficult to heal, and ulcer relapse is more likely in smokers. These clinical observations may be explained by the adverse effects that smoking has on mucosal aggressive and protective factors. Of the aggressive factors, smoking appears to have no consistent effect on acid secretion. However, smoking impairs the therapeutic effects of histamine-2 antagonists, may stimulate pepsin secretion, promotes reflux of duodenal contents into the stomach, increases the risk for and harmful effects of H. pylori, and increases production of free radicals, vasopressin, secretion by the pituitary, secretion of endothelin by the gastric mucosa, and production of platelet activating factor. Smoking also affects the mucosal protective mechanisms. It decreases gastric mucosal blood flow and inhibits gastric mucous secretion, gastric prostaglandin generation, salivary epidermal growth factor secretion, duodenal mucosal bicarbonate secretion, and pancreatic bicarbonate secretion. These adverse effects of smoking on aggressive and protective factors quality it as an important contributor to the pathogenesis of peptic ulcer disease and indicate that smoking plays a significant facilitative role in the development and maintenance of peptic ulcer disease.
 ...
PMID:Is smoking still important in the pathogenesis of peptic ulcer disease? 947 20

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.
 ...
PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84