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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With reference to the case-histories of nine patients with necrosis of the gastric wall and to other data culled from the literature, the hypothesis is advanced that occasionally the gastric ulcer may be the result of ischemia of the lesser curvature caused by the devascularization which is part of the HSV procedure, and that such an ulcer and necrosis of the gastric wall are both consequences of ischemia, differing only in degree.
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PMID:Ulceration and necrosis of the gastric wall after highly selective vagotomy. 90 Sep 56

Ligation of the left gastric and right gastroepiploic arteries and veins resulted in chronic gastric ulcer formation in the rat. Linear mucosal corpus hemorrhages appeared within 8 hr of ligation. By 2 days large corpus hemorrhagic erosions were present. A single, large ulcer involving nearly the entire corpus was present at 3-5 days. In the ulcerated area the mucosa and muscularis mucosae were destroyed, thick granulation tissue filled the submucosa and the muscularis propria was severely damaged. Progressive healing occurred thereafter and 75% of the ulcers healed completely grossly in 2-8 weeks. Histologic studies showed that healing and mucosal regeneration occurred by the outgrowth of a layer of cells from the adjacent intact epithelium extending over the surface of the ulcer. Invaginations from this covering layer of cells formed a glandular mucosa composed of mucous cells. Later parietal and chief cells appeared, and eventually (6 months) a normal corpus-type mucosa covered the entire corpus. With time smooth-muscle fibers appeared in the outer half of the dense submucosal granulation tissue and eventually a normal muscularis mucosae, submucosa, and muscularis propria were present (6-12 months). These studies show that: (1) ischemia can give rise to chronic gastric ulcer, and (2) all elements of the gastric wall, including the mucosa, the muscularis mucosae, and the muscularis propria can fully regenerate.
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PMID:Experimental chronic gastric ulcer due to ischemia in rats. 116 18

The most important complications after open heart surgery are neurological, gastrointestinal (GI), and renal complications. New neurological deficits may occur in 1%, and neuropsychiatric alterations may be observed in 40%. In 6% peripheral neurological damage occurs. Endoscopy in all patients whose clinical history suggests signs of gastric ulcer disease, and perioperative H2-blocking therapy are effective in reducing severe GI bleeding to 1%. Small-bowel ischemia is a rare but high risk complication. Hepatitis due to homologous blood transfusion is as low as 2%-3%. Postoperative renal insufficiency occurs in 1% needing hemodialysis. Good hemodynamic condition during and after surgery reduces the frequency of extracardiac complications as well as the reduction of use of homologous blood transfusions for open heart surgery.
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PMID:[Non-cardiac complications after open heart surgery]. 149 16

The role of tissue-type plasminogen activator (t-PA) was investigated in the gastric ulcer formation induced by microvascular derangement. The rat stomach was exposed and repeated electrical stimuli (irritation) were applied on the small arterial wall close to the lesser curvature to induce mucosal ischemia followed by hyperemia. The t-PA activity in the regional blood of the stomach was significantly elevated as early as 5 min after the irritation. Immunohistochemical study using anti-t-PA monoclonal antibody revealed that t-PA was detectable in the endothelial cells of capillaries and collecting venules, suggesting the involvement of endothelium-mediated fibrinolytic activity in the irritation-induced ulcer formation. Pretreatment of SOD or allopurinol significantly attenuated the irritation-induced t-PA activation, suggesting that the t-PA activity was modulated by xanthine oxidase-associated superoxide anions. CV-6209, a selective antagonist of platelet-activating factor (PAF), also prevented the activation of t-PA as well as ulcer formation, providing a concept that PAF may be associated with the local fibrinolytic activation which may cause hemorrhagic changes in the gastric mucosal microvasculature. The present study supports the hypothesis that increased t-PA activity may reflect the microvascular endothelial damages caused by vasomotor derangement and suggests that oxygen-derived free radicals may participate in the regulation of endothelium-derived fibrinolytic activities in the mucosal microvasculature.
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PMID:Involvement of superoxide anion and platelet-activating factor in increased tissue-type plasminogen activator during rat gastric microvascular damages. 165 Sep 66

Gastric ulceration after fundoplication for gastroesophageal reflux is relatively uncommon, occurring in 1% to 3% of cases. During the period 1974 to 1979, approximately 100 modified Belsey fundoplications were performed at McMaster University Medical Centre. In four patients gastric ulceration developed after the surgery. In all cases the ulcers were located in the proximal stomach, an unusual site. Published reports of gastric ulceration after fundoplication were reviewed, special attention being given to the cause. The authors conclude that local ischemia and mechanical trauma are important in the development of ulceration, which can occur as early as one week after fundoplication. The detection of ulcers requires awareness of the condition and special attention to the symptoms. Because the gastric anatomy is altered by the fundal wrap, the area can be visualized more easily by double-contrast barium studies than by endoscopy.
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PMID:Gastric ulceration after fundoplication. 173 87

In this article, the evidence for the involvement of free radicals in some of the gastrointestinal disorders is reviewed. Oxygen radicals are partially reduced oxygen species that include superoxide, and hydroxyl radicals, and hypophthalous acids. Most cells possess numerous antioxidant enzymes and scavengers to protect themselves from these injurious agents; the rate of production of reactive oxygen metabolites may exceed the capacity of the antioxidant defenses thus resulting in tissue damage. The gastrointestinal tract is particularly well endowed with the enzymatic machinery necessary to form large amounts of oxygen radicals. Sources of radicals in the gastrointestinal tract include mucosal xanthine oxidase and NADPH oxidase found in the resident phagocytotic leukocytes (macrophages, neutrophils, eosinophils) of the lamina propria. Other sources of oxygen radicals in the gastrointestinal tract involve ischemia and reperfusion, drug ingestion, diet and radiation therapy. Recent studies have demonstrated the involvement of oxygen radicals following active episodes of small-intestinal ischemia, ulcerative colitis, pancreatitis and gastric ulcer. In contrast to cell antioxidants, control of tissue free radical levels is now pharmacologically feasible and perhaps justified for specific diseases. However, carefully designed and controlled clinical trials are needed.
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PMID:Oxygen radicals: their role in selected gastrointestinal disorders. 186 20

In studying the side effects of sclerosants injected into the gastric submucosa in dogs (N = 7), we noted that 3 ml of absolute ethanol induced a large gastric ulceration. We describe the time course of change in the ulcer size, and suggest that such ulceration can be used for the endoscopic assessment of factors important in ulcer genesis and healing. Endoscopic reflectance spectrophotometric measurement of indices of mucosal hemoglobin concentration (IHB) and oxygen saturation (ISO2) were performed in a separate group of dogs (N = 4) with ethanol-induced gastric ulceration. We found a significant difference (p less than 0.05) in IHB and ISO2 immediately before (97 +/- 8 and 37 +/- 3, respectively) and after (138 +/- 7 and 21 +/- 5, respectively) the ethanol injection. At 24 hours after the ethanol injection, the IHB at the lesion margin (141 +/- 14) was significantly higher (p less than 0.05) than that at the adjacent mucosa (101 +/- 4), whereas the ISO2 measurements were not significantly different in these two locations, 34 +/- 2 and 31 +/- 2, respectively. We conclude that (1) injection of 3 mol of absolute ethanol into the submucosa of the canine stomach provides an animal model of gastric ulceration in which the ulcer can be examined repeatedly with the aid of the endoscope; (2) in this ulcer model, ischemia with congestion (increases IHB, decreases ISO2) precedes the development of gross mucosal ulcerations; and (3) the margin of the established ulceration in this model exhibits hyperemia (increases IHB, normal ISO2) which mimics that of a healing gastric ulcer.
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PMID:Endoscopic assessment of mucosal hemodynamic changes in a canine model of gastric ulcer. 207 Sep 80

The influence of the proximal selective vagotomy (PSV) on the origin and the extent of experimental gastric ulcer were investigated in rats. The lesions of the gastric mucosa were caused in three groups: by stress through swimming-test, by application of phenylbutazone, and by ischemia (ligature of the left gastric and the right gastroepiploic vessels). The PSV practised a protective influence on the pharmacodynamic etiology, however, not on the stress ulcer. The areas of the ischemic gastric ulcers were larger on an average of 40% after PSV than in the control animals. The difference was not statistically significant. In case the PSV caused besides hyposecretion and hypo-acidity even passive hyperemia caused in the denervated part of the stomach then these did not produce any sufficient defence against the origin of stress ulcers and ischemic lesions.
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PMID:[The effect of proximal selective vagotomy on experimental gastric mucosal lesions in the rat]. 222 3

Rat gastric mucosal blood flow, hydrochloric acid (HC1) secretion, and morphological changes of parietal cells were studied by light and electron microscopy using histochemical techniques. Mucosal blood flow of restrained rats was remarkably decreased compared with that of control rats, whereas the acetylcholinesterase activity, demonstrated by the method of Karnovsky and Roots, was significantly increased especially near the ulcer. In contrast, the differences in volume, acidity and acid output of gastric juice were not significant between control and restrained rats. Hypersecretion of HC1 induced by a parasympathetic stimulant, bethanechol, was inhibited by blood loss or infusion of cytochalasin B, an actin depolymerizing agent. 14C-aminopyrine accumulation in the primary cultured parietal cells was decreased by the treatment with hypoxia and cytochalasin B. These treatments also prevented the increase of 14C-aminopyrine accumulation induced by bethanechol. Actin filaments were evident in the cytoplasm of the parietal cells, particularly around the intracellular canaliculi and beneath the plasma membrane using the FITC-labeled phalloidin reaction and transmission electron microscopic observations of uranyl acetate block stained preparations following heavy meromyosin decorations. Ultrastructural studies of the parietal cells in restrained rats revealed that intracellular canaliculi were dilated with loss of microvilli. Actin filaments were noted to be disassembled, and granular with focal aggregation of actin filaments. Hypoxic vacuoles were also found in the cytoplasm. Treatments with blood loss and cytochalasin B infusion in the in vivo model, and hypoxia and cytochalasin B in the in vitro model, resulted in the similar changes. These observations indicate that actin filaments in the parietal cells of restrained rats may be depolymerized by ischemia. As the result, HC1 secretion would not be enhanced even if the parasympathetic nerves are excessively stimulated in the gastric mucosa. Thus, disturbances of the gastric mucosal microcirculation are considered to be important in the pathogenesis of the stress-induced gastric ulcer.
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PMID:[Studies on the mechanism of restraint-induced gastric ulcer--with special reference to mucosal ischemia and gastric secretion]. 232 29

Various blood flow disturbances in intraabdominal digestive organs were studied clinically and experimentally from a viewpoint of vascular surgery. Acute gastric mucosal lesion may occur due to ischemia and reperfusion injury of the gastric mucosa. Bleeding from stomach ulcer may be rarely caused by consumption coagulopathy along with aortic aneurysm. Heparin therapy was successful to interrupt it. Gastrectomy is not indicated for such condition but aneurysm should be repaired. Portal vein reconstruction for the radical resection of hepatic, biliary and pancreatic cancers should be carefully made, because early or late stenosis occurs frequently, and they may connect to early or late morbidities or mortalities. On the other hand, resection and replacement of the suprarenal vena cava invaded by the retroperitoneal malignant tumor may be safely carried out. For the acute mesenteric arterial occlusion, early diagnosis and arterial reconstruction are essential to save catastrophe. Positive Doppler sound on the vasa recta seems to be the most reliable parameter for assessing bowel viability. Approach from the proximal large arteries is recommended for uncontrollable intraperitoneal bleeding.
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PMID:[Blood flow disturbance in digestive organs--a viewpoint of vascular surgery]. 258 8


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