摘要
本文以无水乙醇灌胃诱发大鼠急性胃粘膜损伤为模型,观察胃粘膜损伤前后以及应用木同剂量胶态次枸橼酸铋(De-Nol)后胃粘膜损伤指数计分和胃粘膜病理组织学改变,并测定胃酸分泌量、胃粘液分泌量、胃粘膜Na^+,K^+ATP酶活力以及不同组动物血浆6-keto-PGF_(l1)内皮素(ET)含量的变化,试图从多方面探讨胶态次枸橼酸铋在抗粘膜损伤中的作用及机制。结果:次枸橼酸铋能有效减轻由无水乙醇造成的胃粘膜病理组织学改变,使损伤指数计分降低,粘膜分泌增加,胃牯膜Na^+.K^+.ATP酶活力上升,并可抑制由于牯膜损伤造成的血浆PGI_2的下降和ET水平的升高,但其对胃酸分泌无明显影响。由此推断,次枸橼酸铋的抗损伤机制与提高血浆PGI_2水平、降低ET、激活Na^+.K^+.ATP酶活力和促进粘液分泌有关,而与抑酸作用无关。
Background/Aims: To evaluate the mechanism of the protective effect of CBS on gastric mucosa. Methods: Animal model of acute gastric mucosa injury was induced by 100% ethanol and different doses of CBS were given orally. Following investigations were made: Na+-K+-ATPase activity of gastric mucosa, serum concentrations of 6-keto-PGF1x,, endothelin, secretions of gastric acid and mucus, and the pathologic changes of optical microscope, scanning electro-microscope, and transmissive electromicroscope. Results: CBS could decrease index of gastric mucosa injury, lessen the pathologic injury, decrease serum concentration of endothelin, and increase serum concentration of 6-keto-PGF1x Na+-K+-ATPase activity in gastric mucosa and secretion of gastric mucus, but the secretion of gastric acid has no change. Conclusion: CBS has preventive effect against acute gastric mucosa injury, the mechanism may relate to multiple factors mentioned above.
出处
《胃肠病学》
1996年第2期98-102,共5页
Chinese Journal of Gastroenterology
