Prostaglandin protection against hemorrhage-induced gastric stress ulceration in the rat

It is shown that in patients with ulcer disease endogenous biosynthesis of prostaglandins E and F2~ in gastric and duodenal mucosa is suppressed. In patients treated with Venter (sucralfat), ulcer healing is accompanied by enhanced prostaglandin production in both scar tissue and unaffected areas. Stimulation of prostaglandin E and F2, " synthesis in the gastroduodenal mucosa followed by activation of their cytoprotective effect in the gastrointestinal system is a key mechanism underlying the effect of Venter.

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“…The intensity of PG synthesis in the gastric mucosa can be evaluated by PG secretion in gastric juice [2,9]. As seen from Table 1 and Fig.…”

Section: Resultsmentioning

confidence: 99%

Gastroduodenal mucosa prostaglandins participate in realization of the effect of the antiulcer drug venter

et al. 1998

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High systemic HCO 3 − and topical 16,16-dimethyl-PGE2 protect gastric mucosa against luminal acid by enhancing its preepithelial buffer capacity

1996

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Systemic metabolic alkalosis and topical prostaglandins protect the gastric mucosa against luminal acid. This study investigates whether this protection is mediated by increased epithelial HCO3(-) secretion with resultant alkalization of the pre-epithelial mucus-HCO3(-) buffer layer. surface pH of chambered ex vivo rat gastric epithelium was measured with liquid sensor pH microelectrodes during luminal perfusion of increasing acidities (0, 10, 30, 50, 100 mM HCL). The experimental groups were: (1) control, (2) topical 16,16-dimethyl-PGE2 treatment, (3) high-HCO3(-) metabolic alkalosis, and (4) low HCO3(-) respiratory alkalosis. The gastric mucosa of PGE2-treated and high-HCO3(-) alkalotic rats tolerated significantly better luminal acid than that of controls, but the tolerance of low-HCO3(-) alkalotic rats was significantly impaired. There was a significant correlation between arterial HCO3(-) concentration (but not arterial pH) and surface pH (r = 0.81, P < 0.01). This suggests that the gastric mucosa against luminal acid are, at least in part, mediated by enhanced buffer capacity of the pre-epithelial mucus-HCO3(-)layer.

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Experimental studies on the prediction and prevention of stress ulcers using tonometry, reflectance spectrophotometry and oxygenated perfluorochemicals

Matin

Baba

Choudhury

1991

The Japanese Journal of Surgery

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The present study investigates whether oxygenated perfluorochemicals protect the gastric mucosa against hemorrhage-induced stress ulceration. The influence of oxygenated perfluorochemicals on both macroscopic and microscopic lesion formation, gastric intramural pH, index of oxygen saturation and index of hemoglobin saturation of the gastric mucosa was studied. To assess the severity of gastric mucosal ischemia, intramural pH was directly measured using a pH sensitive microelectrode and indirectly by utilizing hollow viscus tonometry, and the indices of oxygen saturation and hemoglobin saturation were measured by reflectance spectrophotometry. Oxygenated perfluorochemicals (30 ml/kg/h) significantly protected the gastric mucosa against both gross (lesion index 0.85 +/- 0.2 vs 2.23 +/- 0.31) and microscopic (lesion index 0.52 +/- 0.02 vs 2.04 +/- 0.03) injuries. This protection was associated with a significantly decreased acidification of the mucosa during shock (intramural pH 7.24 +/- 0.02 vs 6.97 +/- 0.02) and significantly increased oxygen saturation of the gastric mucosa (30 +/- 6 vs 5 +/- 2). These data indicate that topical oxygenated perfluorochemicals protect the gastric mucosa against mucosal damage provoked by hemorrhagic shock, and this protection seems to be mediated by an increased oxygen saturation of the gastric mucosa. Tonometry and reflectance spectrophotometry thus are able to predict the critical level of gastric mucosal ischemia.

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Prostaglandin protection against hemorrhage-induced gastric stress ulceration in the rat

Cited by 10 publications

References 28 publications

Gastroduodenal mucosa prostaglandins participate in realization of the effect of the antiulcer drug venter

Gastroduodenal mucosa prostaglandins participate in realization of the effect of the antiulcer drug venter

High systemic HCO 3 − and topical 16,16-dimethyl-PGE2 protect gastric mucosa against luminal acid by enhancing its preepithelial buffer capacity

Experimental studies on the prediction and prevention of stress ulcers using tonometry, reflectance spectrophotometry and oxygenated perfluorochemicals

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