Arakawa T, Kobayashi K, Nakamura H, Chono S, Yamada H, Ono T, Yamamoto S
Gastroenterol Jpn. 1981;16(3):236-41. doi: 10.1007/BF02815803.
We investigated the effect of stress on the prostaglandin E2 levels in rat gastric mucosa. In untreated controls, prostaglandin E2 levels were higher in the antral than the fundic mucosa. Stress experiments showed tht 30-min stress induced no gastric lesions but effected a significant (p less than 0.05) increase in antral prostaglandin E2: after 7-hr stress exposure, hemorrhagic lesions and prostaglandin E2 levels significantly (p less than 0.05) below normal control values were noted. The formation of HCl-induced gastric mucosal lesions was markedly inhibited if 30-min stress preceded HCl-administration. The infusion of 5 microgram/kg 16, 16-dimethyl prostaglandin E2 prior to 7-hr stress exposure inhibited ulcer formation markedly. Our results suggested that stress-induced decrease in intramucosal prostaglandin E2 plays an important role in the pathogenesis of stress ulcer formation.
我们研究了应激对大鼠胃黏膜中前列腺素E2水平的影响。在未经处理的对照组中,胃窦黏膜中的前列腺素E2水平高于胃底黏膜。应激实验表明,30分钟的应激未诱发胃部病变,但导致胃窦前列腺素E2显著升高(p<0.05);在7小时的应激暴露后,出现了出血性病变,且前列腺素E2水平显著低于正常对照值(p<0.05)。如果在给予盐酸前进行30分钟的应激,则盐酸诱导的胃黏膜病变的形成会受到明显抑制。在7小时的应激暴露前输注5微克/千克的16,16-二甲基前列腺素E2可显著抑制溃疡的形成。我们的结果表明,应激诱导的黏膜内前列腺素E2减少在应激性溃疡形成的发病机制中起重要作用。