Isobe Y, Hirose-Kijima H, Muramatsu M, Aihara H
Department of Pharmacology, Taisho Pharmaceutical Co., Ltd., Saitama, Japan.
Arch Int Pharmacodyn Ther. 1988 Sep-Oct;295:270-81.
The effects of gastric secretagogues on 0.6N HCl-induced gastric lesions and gastric mucosal prostaglandin E2 (PGE2) contents were investigated in rats. Secretagogues such as histamine (Hist) and amogastrin (Gast) significantly inhibited the formation of gastric lesions induced by 0.6N HCl. The time course of the gastric protective effect of these secretagogues paralleled the increase of gastric acid secretion. This increase was due to the increase in acidity, not to the volume of the gastric juice. The gastric protective effects of Hist and Gast were inhibited by pretreatment with cimetidine, timoprazole and indomethacin. Hist and Gast caused an increase of PGE2 contents in gastric mucosa. These increases were inhibited by the administration of cimetidine and timoprazole. Carbachol (CCh), however, did not have any gastric protective effect; nor did it have any effect on PGE2 contents. CCh caused an increase of acid secretion due to the increase of the volume of gastric juice, but not to an increase in acidity. These results suggest that the gastric protective effect of Hist and Gast, induced by the increase of acidity in gastric juice, is due to the endogenous PGE2 synthesized by the stimulation of acid in the gastric mucosa.
研究了胃促分泌素对0.6N盐酸诱导的大鼠胃损伤及胃黏膜前列腺素E2（PGE2）含量的影响。组胺（Hist）和蛙皮促胃液素（Gast）等促分泌素显著抑制0.6N盐酸诱导的胃损伤形成。这些促分泌素的胃保护作用的时间进程与胃酸分泌的增加平行。这种增加是由于酸度的增加，而不是胃液体积的增加。西咪替丁、替莫拉唑和吲哚美辛预处理可抑制Hist和Gast的胃保护作用。Hist和Gast可使胃黏膜中PGE2含量增加。西咪替丁和替莫拉唑给药可抑制这些增加。然而，卡巴胆碱（CCh）没有任何胃保护作用；它对PGE2含量也没有任何影响。CCh由于胃液体积增加导致胃酸分泌增加，但不是由于酸度增加。这些结果表明，胃液酸度增加诱导的Hist和Gast的胃保护作用是由于胃黏膜中酸刺激合成的内源性PGE2所致。
