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

A case of the hemorrhagic gastric ulcer and post-operative stomal ulcer associated with the consumption coagulopathy in the dissecting aortic aneurysm is presented. A 68 year old man, who had diagnosed as having the dissecting aortic aneurysm (DeBakey III) in 1985 and had been attending to our hospital as an outpatient since then, was admitted to our hospital because of the hemorrhagic gastric ulcer on July 3rd, 1987. Although the wide resection of stomach was performed after the admission, the hemorrhagic stomal ulcer was developed 4 weeks after the operation. The administration of heparin in addition to antacids to improve the consumption coagulopathy, having been caused by thrombus formation in the aneurysm, was effective in control of the hemorrhage and also making the stomal ulcer scarred. It is suggested that ischemia of the stomach mucosa, which seemed to have been induced by the dissecting aortic aneurysm, was responsible for the development of the ulcers in this case and the hemorrhage from them was caused mainly by the consumption coagulopathy derived from thrombus formation in the aneurysm.
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PMID:[Hemorrhagic gastric ulcer associated with consumption coagulopathy in the dissecting aortic aneurysm--a case report]. 281 45

Gastric ulceration has been induced after stress, combining 24 h of fasting and 48 h of restraint in 9 groups of 20 rats with or without a pyloroplasty or a pylorojejunostomy combined with atropine and gastric infusion of NaHCO3 or taurocholic acid. After death or sacrifice at 48 h, ulcer index and blood in the jejunum were determined. Gastric mucosal blood flow was measured semi-continuously by a laser Doppler velocimeter. There were 45% deaths after 48 h of restraint alone, and 70% in the group combining pylorojejunostomy with taurocholic acid. Mortality was lower (p less than or equal to 0.01) pylorojejunostomy alone and more significantly so (p less than or equal to 0.001) when associated with NaHCO3. There was no death when NaHCO3 and atropine were combined with restraint. The mucosal blood flow increased significantly during the first 12 h of restraint in the taurocholic acid group. Both groups with NaHCO3 had mucosal blood flows similar to the controls. Gastric acid and gastric emptying, mucosal ischemia and bile reflux are joint factors inducing gastric stress ulcer. The 100% survival and the low ulcer index after a treatment by atropine and gastric infusion of NaHCO3 suggest that these well-known drugs should be used more frequently.
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PMID:Gastric stress ulcer of the rat: relative contribution of the pyloric sphincter, HCO3- bile reflux and mucosal blood flow. 301 38

Four middle-aged women presented with long histories of severe progressive weight loss and chronic abdominal pain. Endoscopically atypical gastric ulcers were identified in all; the ulcers were multiple and antral in location, with irregular shapes, sloping edges, and whitish sclerotic bases, and were surrounded by mottled and erythematous mucosa containing numerous superficial erosions. They did not heal with conservative therapy. All 4 patients were found to be suffering from chronic mesenteric vascular insufficiency. Balloon dilatation of the superior mesenteric artery in one and surgical revascularization in the others resulted in progressive clinical improvement and healing of the ulcers. The striking feature in these patients with mesenteric ischemia was the finding of gastric ulcers with a morphology different from the ordinary gastric ulcer, which healed only with revascularization. Future observation of similar lesions should suggest the possible diagnosis and expedite early treatment of mesenteric insufficiency in patients with this disorder.
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PMID:Chronic mesenteric vascular insufficiency with gastric ulceration. 377 Mar 79

Comparative vertebrate anatomy shows that acid secretion and wall stress processes typically occur in different compartments. In the human single-chamber stomach both processes are physiologically separated in time. If both processes take place in one hollow organ at the same time, focal ischemia will occur. Using the microsphere technique a submucous steal-phenomenon, which the effect is due to, has been reproduced experimentally. A network model of the human gastric vascular bed produces borderline infarcts at the preferred sites of human gastric ulcer.
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PMID:[Functional anatomy of stomach circulation: localizing factors in the pathogenesis of stomach ulcer]. 395 81

Gastric antral lesions were produced with hemorrhages by vascular ligation-induced ischemia in the prepyloric regions in rats. Additional treatments with intraluminal acid application and indomethacin markedly aggravated the lesions. Histological examination showed that the incidence of ulcers which penetrated the muscularis mucosae was nearly 100% upon treatment with a combination of acid, indomethacin and ischemia. This model provides a useful tool for studying gastric ulcer etiology.
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PMID:Gastric antral ulcers induced by a combination of acid, indomethacin and ischemia in rats. 403 59

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. If they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acid-pepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.
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PMID:The pathophysiology of peptic ulcer disease. 405 22

The purpose of the present study was to elucidate the effect of duodenal juice on development of gastric ulcer, in relation to changes of lipid composition and energy metabolism of the gastric mucosa in dogs. For regurgitation of duodenal juice and stagnation of gastric contents in the stomach, the duodenum was constricted below the papilla of Vater, accompanying with pyloroplasty and upper gastro-jejunostomy. Furthermore, to induce ischemia in the gastric mucosa, 0.5 ml of 1% formalin solution was injected into a descending branch of the left gastric artery. Three weeks later, U1 II-III gastric ulcer developed at the formalin injected area with severe gastritis but not with hyperacidity, and the histologic findings were similar to the one of a human gastric ulcer with hypoacidity. On assay of lipid composition in the gastric mucosa, lecithin decreased and both lysolecithin and NEFA increased, showing that lecithin of the gastric mucosa was decomposed by phospholipase A2 of the duodenal juice. In the gastric mucosa, ATP and energy charge decreased, and AMP and lactate increased, indicating that the energy metabolism was led to anaerobic glycolysis. These results revealed that the gastric mucosa becomes very fragile when duodenal juice regurgitates into the stomach and that gastric ulcer may develop even without hyperacidity when the microcirculation is disturbed in this condition.
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PMID:Effect of duodenal juice on pathogenesis of gastric ulcer. 683 47

The gastric mucosal barrier is that property which defends against acid and which impedes diffusion of acid from the lumen into the mucosa. The disappearance of luminal H+ is linearly related to luminal (H+) both in the normal stomach and in stomachs exposed to barrier breakers. The latter invaribaly produce anatomic evidence of surface cellular injury. Strong direct evidence for back diffusion of luminal H+ derives from the recent demonstration of a highly significant correlation between the disappearance of luminal H+ and the pH of the lamina propria measured by an implanted microelectrode. The permeabilities of the antrum and fundus to H+ differ from each other in the same species and in different species. Gastric ulceration does not occur in the absence of luminal acid and is not dependent upon the absolute loss of H+ from the luminal solution. Mucosal ischemia induced by hemorrhage reduces tolerance against ulceration as does inhibition of acid secretion, acidification of the tissue caused by absence of nutrient bicarbonate, inhibition of carbonic anhydrase, and blockade of anion exchange by SITS. A tentative schema is proposed by which defense against luminal acid is accomplished in gastric mucosa.
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PMID:The gastric mucosal barrier and ulceration. 699 46

Numerous factors are involved in the pathogenesis of gastric ulcer. Possibilities under discussion are acid back diffusion, a reduction in the quality of the gastric mucus, and vascular factors that give rise to local ischemia. One hypothetical model presented for consideration, is based on the notion of an "internal leak", as a result of which acid escapes out of the parietal cells directly into the interstitium. Using the cationic dye acridine orange in cats, it has been possible to show, in particular after prior stimulation with stimulation with histamine and carbachol, but not with pentagastrin, that a microfocal accumulation of the dye in the interstitium can indeed be found. Under conditions of hypoxia, this phenomenon was not observed. In view of the specific properties of the dye, it may be concluded that, under certain conditions, acid substances can indeed diffuse out of the parietal cells into the interstitium. this animal model offers distinct findings compatible with the pathogenetic concept of an "internal leak".
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PMID:Experimental evidence for an "internal leak" of cat gastric mucosa after stimulation with histamine and carbachol. 708 86

1) One of the possible etiologies of gastric ulcers which frequently occur in the lesser curvature is ischemia or necrosis of the gastric wall, which stem from increased rigidity of the blood vessel walls, mainly caused by dysfunction of sympathetic nerve. 2) The main blood supply to the gastric wall is controlled by gastric arteries, with the gastroepiploic arteries playing only an auxiliary role. 3) It should be noted that gastric bleeding or mucosa necrosis will occasionally occur in some cases of SPV or SV. 4) It was established that experimental rat ulcers of UL-II or UL-III severity which are analogous to human gastric ulcer are produced by cold restricted rat combined with ligation of the gastric arteries (MOHRI's method).
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PMID:New aspects in the pathogenesis of gastric ulcer. 738 52


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