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)

During the last decade, evidence increased that microcirculatory disorders play a pivotal role in the development of mucosal injury, and, hence, formation of gastric ulcer. Mucosal microcirculation is altered at least by two distinct mechanisms: Stimulation of acid secretion leads to a rise of blood flow in the acid-secreting areas, and, concomitantly, due to a steal-phenomenon to a decrease of mucosal capillary perfusion of the antrum, which results in temporary ischemia. In addition, surface noxae-induced release of potent mediators, such as histamine, leukotrienes, thromboxane, platelet-activating factor and reactive oxygen metabolites cause vasoconstriction, capillary stasis and increase of microvascular permeability (loss of endothelial integrity), which aggravate mucosal injury. Therefore, therapeutic strategies should consider leukotriene-synthesis inhibitors, histamine-, thromboxane- and platelet-activating factor receptor antagonists, oxygen radical scavengers, as well as counteracting mediators and hormones, such as prostaglandins and somatostatin, inasmuch as these compounds have been shown to additionally prevent mucosal microvascular injury, in particular capillary perfusion failure and loss of endothelial integrity, during gastric ulcer formation.
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PMID:[Microcirculation of gastric mucosa in pathogenesis of stomach ulcer]. 751 63

Blood flow plays an important role in protection of normal gastric mucosa and in the protection and healing of damaged mucosa. Blood flow contributes to protection by supplying the mucosa with oxygen and HCO3-, and by removing H+ and toxic agents diffusing from the lumen into the mucosa. Low mucosal blood flow predisposes to injury, whereas high blood flow protects against injurious agents. Superficial mucosal damage is followed by increased blood flow which supports the healing process and prevents superficial lesions from developing into deep ones. The hypermic response increases the supply of HCO3- to the mucosa and increases the resistance of the injured mucosa against back diffusing H+ and aggressive drugs such as ethanol (adaptive protection). Mucosal ischemia contributes to gastric ulceration in various clinical conditions such as hemorrhagic shock, stress, aorta aneurysm and after proximal gastric vagotomy. Blood vessels are damaged in gastric ulcers. During ulcer healing blood flow returns to normal. Stimulated or inhibited angiogenesis in the granulation tissue effects the healing of a gastric ulcer.
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PMID:The role of blood flow in gastric mucosal defence, damage and healing. 753 77

Case reports of five patients with pneumatosis intestinalis diagnosed by computed tomography (CT) are presented. Etiology, differential diagnoses, and clinical consequences arising from CT imaging are discussed. In four of the patients, pneumatosis was found to be secondary to gastric ulcer, colon carcinoma, metastasis in the mesentery, and trauma-induced mesenteric ischemia. In one patient, the etiology remained elusive. Using CT, both the extent and the distribution pattern of pneumatosis could be depicted, allowing for differentiation of primary and secondary forms and assessment of prognosis. Evaluation with a lung window is a pre-requisite for reliable diagnosis of pneumatosis with CT. The presence of gas in the mesenteric or portal venous system in mesenteric ischemia is indicative of an unfavorable prognosis.
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PMID:Computed tomography in pneumatosis intestinalis: differential diagnosis and therapeutic consequences. 858 Jul 46

A new model of gastric ulcer involving damage to the muscularis mucosae was developed by clamping the celiac artery in rat to induce ischemia-reperfusion (I-R) injury. Although erosions with falling off of the gastric mucosa were observed immediately, 24 and 36 hours after the I-R, gastric ulcers involving the injury of muscularis mucosae were observed in the area of gastric glands at 48 and 72 hours after initiation of injury. Administration of omeprazol, a proton pump inhibitor, or pentoxifylline, an anti-leukocyte drug, just after the initiation of injury significantly decreased the total area of ulcers at 72 hours. A combination of omeprazol and pentoxifylline was more effective than either drug alone. An anti-leukocyte adhesion molecule (anti-CD18 antibody) also showed significant inhibitory effect on the development of ulcers at 72 hours and the infiltration of leukocytes into both submucosa and mucosa. These results indicate that in our model, gastric acid together with leukocytes contribute to the development of ulcers following erosions. This model may be used to investigate the mechanisms of the development of gastric ulcer and evaluate antiulcer drugs in a preclinical setting.
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PMID:A new gastric ulcer model induced by ischemia-reperfusion in the rat: role of leukocytes on ulceration in rat stomach. 891 34

We investigated the role of endogenous gastric acid in the development of gastric ulcer from erosion induced by ischemia-reperfusion of the celiac artery in the rat. A half-hour clamping of the celiac artery (ischemia) caused acute gastric erosions 1 hour after reperfusion and such acute injuries progressed to ulcers 48-72 hours after reperfusion without any necrotizing agents. Gastric acid secretion decreased immediately after ischemia and didn't recover until 12 hours after reperfusion. Intraperitoneal administrations of cimetidine (100 mg/kg, every 12 hours) or omeprazole (30 mg/kg, every 24 hours) were started at 1, 6, or 12 hours after reperfusion. When administrations were started 1 hour after reperfusion, both drugs significantly decreased the total damaged area and prevented the progression of gastric erosions to ulcers. However, administrations started 6 or 12 hours after reperfusion failed to inhibit the total damaged area and to prevent ulcer formation. These results suggest that endogenous gastric acid may play an important role in the progression of gastric erosions to ulcers although ischemia itself reduces acid secretion. Furthermore, treatment with anti-acid-secretory drugs in the early stage of mucosal damage may be important for the prevention of ulcer.
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PMID:The role of endogenous acid in the development of acute gastric ulcer induced by ischemia-reperfusion in the rat. 945 May 9

Recently, the state of cyclooxygenase (COX) mRNA expression has been reported in an acetic acid-induced chronic gastric ulcer model of mice. However, the time course of COX expression during the developmental stage and the subsequent repair process of acute gastric injury is not well understood at present. In this study, we quantitatively investigated the time course of the level of COX-2 and -1 mRNA expression from the developmental stage through the healing stage in ischemia-reperfusion (I-R)-induced acute gastric damage. COX-2 mRNA was expressed at low or undetectable levels in the normal gastric tissues of control rats. The COX-2 expression between 6 and 48 h following I-R was higher than that of the control gastric tissues; the histological findings were erosion during 1-36 h and transitional appearance from erosion to ulcer at 48 h. The maximum expression of COX-2 mRNA was recorded at 24 h (approximately 200-fold elevation). The COX-2 message was very low or undetectable at 72 h (ulcer stage) and at 96 and 120 h (healing stage of ulcer) after I-R. The level of COX-1 mRNA remained stable through all stages of acute gastric damage. These results are potentially useful for understanding the role of COX and evaluating the effects of drugs on expression of COX at various stages of acute gastric injury.
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PMID:Levels of cyclooxygenase-1 and -2 mRNA expression at various stages of acute gastric injury induced by ischemia-reperfusion in rats. 952 28

A new gastric ulcer model was developed by the ischemia-reperfusion procedure in rats. The ischemia-reperfusion was produced by clamping the celiac artery and subsequent removal of the clamp. Until 36 hr after the ischemia, erosive lesions were observed in the gastric glands. However, 48 and 72 hr after the ischemia, gastric ulcers involving damage of muscularis mucosae were observed. Seven days after the ischemia, the injured areas were covered with regenerated mucosa. This model may be useful for investigating the mechanisms of pathogenesis of gastric ulcer and to evaluate efficacy of drugs.
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PMID:[Development of a new gastric ulcer model and the evaluation of drug effects]. 966 85

Submucosal injection of endothelin (ET)-1 induces gastric ulcer. We investigated the roles of neutrophils and adhesion molecules (intercellular adhesion molecule (ICAM)-1 and CD18) in the development of ET-1-induced ulcers in rats. Ulcers were induced by submucosal injection of ET-1. Rats were injected with anti-neutrophil serum or F(ab')2 fragments of irrelevant mouse IgG2a (control), anti-ICAM-1 antibody, or anti-CD18 antibody. Ulcer tissues were subjected to measurement of myeloperoxidase (MPO) activity, ulcer size, and immunohistochemical study. Within 3 hr, arterial vasoconstriction and vascular congestion were observed at sites of ET-1 injection. By 6 hr, vascular congestion had disappeared, and ICAM-1 expression had markedly increased in venules in deep portions of the mucosa and submucosa, accompanied by an increase in the number of CD18-positive neutrophils. By 48 hr, ulcers that extended into the submucosa had developed. In controls, MPO activity gradually increased and was maximal by 6 hr. Neutrophil depletion, and immunoneutralizing of ICAM-1 and CD18 inhibited the increase in MPO activity, and decreased ulcer sizes measured at 48 hr. In conclusion, ET-1 causes ischemia-reperfusion injury, and neutrophil accumulation after reperfusion mediated by the ICAM-1-CD18 pathway may be important in the development of ET-1-induced gastric ulcer.
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PMID:Neutrophil accumulation in development gastric ulcer induced by submucosal injection of endothelin-1 in rats. 1079 48

The rich blood supply of the stomach protects it from ischemia and necrosis. Acute gastric ischemia, an emergency with high mortality, is rare. Atherosclerosis is the leading cause of acute ischemia, and the lesser curvature of the stomach is more vulnerable due to its relatively lesser blood supply. Reduction in gastric blood supply usually presents as chronic disease characterized by gastritis, gastric ulcer, or gastroparesis. Gastroscopy can identify lesions of the gastric mucosa, and angiography demonstrates occluded vessels. Treatment of acute gastric ischemia is surgical, with total gastrectomy preferred over partial resection.
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PMID:[Acute ischemia of the lesser gastric curvature--a rare marker of sclerotic disease]. 1088 78

The diagnosis and management of gastrointestinal complications associated with cardiopulmonary bypass is often hindered by a complicated clinical picture and equivocal examination. To better define the incidence, risk factors, and mortality, we reviewed the records of all patients undergoing cardiopulmonary bypass from 1988 through 1996. The database for this study comprised 14,521 patients who underwent cardiac surgery. The patients (543) with gastrointestinal complications were identified, and those with major complications (166) were individually reviewed. Major complications included pancreatitis, gastritis, laparotomy, gastric ulcer, cholecystitis, colonic perforation, gastrointestinal bleeding, diverticulitis, bowel obstruction, perforation, and visceral ischemia. Our results were the following. 1) Gastrointestinal complications were noted in 3.7 per cent (543) of patients with major complications occurring in 1.2 per cent. In 166 patients, 187 major complications were noted. 2) Visceral ischemia, an infrequent but usually fatal (71%) complication, occurred in 24 (0.17%). 3) Of the ischemic events, 83 per cent (20 of 24) affected the bowel; with the colon involved 80 per cent of the time (16 of 20). 4) Patients with visceral ischemia were more likely to be female (relative risk 2.1), have longer pump times (92.2 versus 74.2), have cardiac procedures other than coronary artery bypass graft (relative risk 2.6), and have end-stage renal disease (relative risk 16.7). We conclude that, given the incidence and mortality related to visceral ischemia, especially to the colon, patients with risk factors (end-stage renal disease, female sex, non-coronary artery bypass graft, and longer pump times) should undergo routine endoscopic examination of the colon early after bypass and when clinically indicated thereafter.
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PMID:Visceral ischemia after cardiopulmonary bypass. 1091 70


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