Increased ex vivo synthesis of prostaglandin E2 by gastric tissue after hemorrhage in rats.
Endogenously synthesized prostaglandins are potential mediators of gastrointestinal mucosal protection. Some data suggest that gastric ulceration caused by stressful stimuli is due to diminished mucosal synthesis of prostaglandins. To examine this hypothesis, we determined the effect of hemorrhage, an ulcerogenic stimulus, on ex vivo production of immunoreactive prostaglandin E2 by gastric tissue in the rat. Macroscopic gastric ulcers were reproducibly observed in Sprague-Dawley rats subjected to hemorrhage (3 ml/100 g body weight). The number of ulcers was linearly related to the duration of shock. Prostaglandin E2 synthesis was significantly increased during in vitro incubation of oxyntic and nonoxyntic stomach tissue excised from rats subjected to hemorrhage for 30 minutes (p less than 0.05). These results indicate that damage to the gastric mucosa in rats subjected to hemorrhage occurs despite augmented endogenous secretion of prostaglandin E2. Mechanisms other than impaired prostaglandin biosynthesis were probably responsible for mucosal injury in this model.
D000818:Animals; D015232:Dinoprostone; D005753:Gastric Mucosa / Q000378:metabolism*; D006471:Gastrointestinal Hemorrhage / Q000378:metabolism*; D008297:Male; D011458:Prostaglandins E / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000378:metabolism*
D011458:Prostaglandins E; D015232:Dinoprostone