Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An ulcer was induced in the anterior wall of the antrum by local injection of acetic acid solution. Carbonized microspheres 15 +/- 5 micrometer in diameter, labeled with 85Sr and 141Ce, were used to measure blood flow in different regions and layers of the stomach wall, and in each sample the mucosa was separated from the muscularis. The radioactivity of a blood reference sample and the tissue sample was determined, and the blood flow was calculated for each tissue sample. Two groups of anesthetized animals were used: animals with normal stomachs given vasopressin and animals with a 1-week ulcer given vasopressin. The vasopressin was administered intravenously over a 20-min period. In animals with normal stomachs and in animals with a gastric ulcer vasopressin was found to decrease the blood flow to the stomach in all areas examined. The presence of a 1-week ulcer in the cat did not seem to influence the effect of vasopressin.
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PMID:Effect of vasopressin on blood flow distribution in the stomach of cats with gastric ulcer. 72 99

A bleeding gastric ulcer was surgically created in 18 dogs, and the left gastric artery was successfully catheterized by percutaneous techniques in 15. Nine of these dogs were treated with vasopressin infusion which did not arrest the hemorrhage. A total of 11 dogs (five of them following unsuccessful vasopressin therapy) underwent embolization with strips of Gelfoam, and hemorrhage stopped in ten. This technique of embolization is concluded to be of value in the management of gastric hemorrhage.
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PMID:Gelfoam embolization of the left gastric artery for bleeding ulcer: experimental considerations. 108 Feb 82

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

The effects of subcutaneous injections of vasopressin in vasopressin-deficient (Brattleboro or DI) rats were observed during nonstress (habituation) and stress (food-restriction) conditions as compared to other rats. Four groups of animals were employed: 1) Long-Evans (LE) rats that were food restricted with no injections (normal control animals), 2) DI rats that were food restricted with no injections, 3) DI rats injected with vasopressin, and 4) DI rats injected with peanut oil (vehicle). The parameters studied were: body weight, food intake, water intake, and gastric ulcer formation. With respect to body weight, water intake, and ulcer formation, two sets of animals emerged. The vasopressin-injected DI rats resembled the LE control rats, whereas the peanut oil-injected DI rats were similar to the DI rats with no injections. The former set of animals showed a higher body weight, reduced water intake, and fewer gastric ulcers than the latter set of animals. Thus the vasopressin-injected DI rats and the LE control rats could cope with the stress of food restriction, but the peanut oil-injected DI rats and the DI rats with no injections could not.
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PMID:Effects of vasopressin replacement during food-restriction stress. 206 79

Two cases of miliary tuberculosis with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) were reported. Case 1. A 70-year-old woman suffering from general fatigue and appetite loss developed neck stiffness and stupor three days after admission. The chest X-ray film showed a miliary pattern in both lungs. The lumber puncture showed high pressure and increased leucocytes in the cerebrospinal fluid. Serum natrium concentration was 113 mEq/L. Tubercle bacilli were seen in the broncho-alveolar lavage fluid by the Ziehl-Nielsen staining. An improvement in electrolytes balance was produced by 2.5% NaCl and antituberculous treatment, then her mental function recovered. Case 2. A 71-year-old man was admitted with gastric ulcer. When he developed dry cough thirty days after admission, the chest X-ray film showed a miliary pattern in both lungs. Acute respiratory failure advanced concomitantly. Tubercle bacilli were seen in the sputum (Gaffky 5) by the Ziehl-Nielsen staining. Antituberculous treatment was started. Although the miliary shadow improved gradually, hyponatremia was rather progressing. The following values for serum constituents were determined: sodium, 118 mEq/L; antidiuretic hormone, 10.3 pg/ml. Antituberculous treatment and supplement of NaCl (10 g/day) improved serum natrium level. He had no mental disturbance in his clinical course. In both cases, thyroid, renal and adrenal function were normal. Systemic edema and dehydration did not exist at the state of hyponatremia, and it was very clear that laboratory data were compatible with SIADH criteria. Miliary tuberculosis is one of the least commonly recognized causes of SIADH.
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PMID:[Two cases of miliary tuberculosis with SIADH]. 279 13

The effects of different doses of Asu(1,7) eel-calcitonin, peripherally injected, on gastric secretion were studied in conscious Brattleboro rats, which are genetically deficient in vasopressin. Moreover, we evaluated the activity of this analogue on gastric ulcer formation by restraint stress. We found that 5 IU/kg Asu(1,7) eel-calcitonin decreased gastric secretion and inhibited the development of stress-induced ulcers in Brattleboro rats. These data suggest that vasopressin does not play a role in the gastrointestinal activity of Asu(1,7) eel-calcitonin.
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PMID:Inhibition of gastric secretion and stress-induced ulcers by intravenous Asu(1,7)eel-calcitonin independent of vasopressin. 362 98

The influence of various ulcerogenic treatments on healing gastric ulcers induced by thermocautery was studied in mice. A low dose of serotonin (5HT) which did not produce ulceration, was found to aggravate gastric ulcers at 15th or 30th day after thermocauterization, but other ulcerogenic treatments including histamine, norepinephrine, vasopressin, acetic acid ingestion and cold-restraint stress did not affect this induced gastric ulcer. Bleeding and ulceration, however, occurred in the gastric glandular portion in addition to thermocauterization ulcer by the treatment of acetic acid ingestion or cold-restraint stress. Histological sections of gastric ulcers (15th and 30th day) 24 hr after 5HT injection, showed severe necrosis of the regenerated mucosal layer. Microvessel structure in the gastric mucosa as revealed by the Indian-ink infusion, showed a local obstruction of blood flow on the edge of ulcers 1 or 3 hr after 5HT injection. Although acetic acid ingestion increased transmucosal fluxes of Na+ and K+, 5HT had no effect on the ion flux in normal mice. Thus the healed ulcer area was resistant to various ulcerogenic stimulants, except for 5HT, and the vasoactive factor of 5HT may be involved in the aggravating process of gastric ulcers induced by thermocautery.
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PMID:Aggravating effect of serotonin on gastric ulceration induced by thermocautery under the healing process in mice. 745 84

Since endogenous vasopressin has been reported to be an aggressor in the gastric mucosa and a vasoconstrictor in the gastric circulation, we investigated the gastric cytoprotective effects of OPC-21268, a newly developed, nonpeptide, orally active vasopressin-1 receptor antagonist, on ethanol-induced gastric injury in rats. The rats were treated with OPC-21268 or placebo 2 hr before ethanol administration, and the gastric mucosa was evaluated macroscopically for ulcer damage, and histologically for gastric mucosal injury. Gastric mucosal blood flow, erythrocyte volume, and erythrocyte velocity were also measured in groups given saline, ethanol alone, and ethanol after OPC-21268. To investigate the role of systemic or locally secreted vasopressin, we measured plasma and tissue (gastric mucosa) vasopressin concentrations after ethanol or vehicle administration. Prophylactic OPC-21268 treatment improved the gastric ulcer score in a dose-dependent manner, and histological examination demonstrated that the drug significantly ameliorated the gastric injury induced by ethanol. The hemodynamic values obtained in the OPC-21268-treated and ethanol-treated group were similar to those in the saline control group, but values were significantly (P < 0.05) higher for gastric mucosal blood flow and erythrocyte velocity and lower for erythrocyte volume compared to the group given ethanol alone. Plasma vasopressin concentrations were not significantly different in the control group and at 15, 30, and 60 min after administration of ethanol. However, ethanol administration caused a threefold increase in gastric tissue vasopressin level (P < 0.05) compared to the control group. These results suggested that OPC-21268 relieved congestive hyperemia in the gastric mucosa and ameliorated the mucosal injury caused by ethanol, probably as a result of inhibition of vasopressin-mediated actions on the stomach. The vasopressin involved was probably generated locally in the gastric mucosa after ethanol administration.
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PMID:Protective effect of a vasopressin-1 selective antagonist, OPC-21268, against ethanol-induced damage of the rat gastric wall. 1008 Jan 41

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

A recalcitrant rheumatoid arthritis patient taking low dose weekly methotrexate was given oral 2-chlorodeoxyadenosine (cladribine) for 8 months in a multicenter trial. He developed dual infections over the course of the trial: disseminated herpes zoster and staphylococcal arthritis of the right elbow. His disseminated herpes zoster started with severe, unremitting abdominal pain caused by a gastric ulcer, followed by disseminated cutaneous herpes, hepatitis, pancreatitis, encephalitis, homonymous hemianopsia, the syndrome of inappropriate secretion of antidiuretic hormone (ADH), and malabsorption. Both the herpes zoster and S. aureus infections required prolonged proper chemotherapies. Serious, complicated viral, bacterial, or other unusual infections should be considered in patients with severe rheumatoid conditions treated with combination immunosuppressive therapy.
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PMID:Disseminated herpes zoster and s. Aureus septic arthritis in a rheumatoid arthritis patient treated with 2-chlorodeoxyadenosine (cladribine) and methotrexate. 1907 80


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