Kauffman G L, Grossman M I
Gastroenterology. 1978 Dec;75(6):1099-1102.
Antral ulcers were produced in unanesthetized rats in 3 hr by simultaneous intravenous administration of acetylsalicylic acid (ASA) and gastric perfusion with 0.15 M HCl. Intravenous infusion of ASA alone or gastric perfusion with HCl alone produced no antral ulcers. Plasma salicylate levels ranged from 250 to 350 microgram ml-1. 16-16 Dimethyl prostaglandin E2 (DMPGE2) (0.04, 0.40, 4.0 microgram kg-1 hr-1) and cimetidine (10, 50 mg kg-1 hr-1) significantly decreased the severity of antral ulcers in a dose-dependent fashion. In a separate group of unanesthetized rats prepared with gastric fistula and pylorus ligation, pepsin output during administration of parenteral ASA and gastric perfusion of HCl was reduced by the highest doses of 16-16 DMPGE2 and cimetidine. However, addition of exogenous pepsin to the HCl perfusate had no effect on the inhibition of ulceration afforded by 16-16 DMPGE2 and cimetidine. We conclude that both 16-16 DMPGE2 and cimetidine protect antral mucosa against injury by parenteral ASA plus topical HCl by some means other than their effect on acid and pepsin output.
在未麻醉的大鼠中,通过同时静脉注射乙酰水杨酸(ASA)和用0.15 M HCl进行胃灌注,在3小时内产生胃窦溃疡。单独静脉输注ASA或单独用HCl进行胃灌注均未产生胃窦溃疡。血浆水杨酸盐水平在250至350微克/毫升之间。16,16-二甲基前列腺素E2(DMPGE2)(0.04、0.40、4.0微克/千克/小时)和西咪替丁(10、50毫克/千克/小时)以剂量依赖性方式显著降低胃窦溃疡的严重程度。在另一组制备有胃瘘和幽门结扎的未麻醉大鼠中,在静脉注射ASA和胃灌注HCl期间,最高剂量的16,16-DMPGE2和西咪替丁可降低胃蛋白酶的分泌量。然而,向HCl灌流液中添加外源性胃蛋白酶对16,16-DMPGE2和西咪替丁对溃疡形成的抑制作用没有影响。我们得出结论,16,16-DMPGE2和西咪替丁通过某种方式保护胃窦黏膜免受静脉注射ASA加局部HCl的损伤,而不是通过它们对胃酸和胃蛋白酶分泌量的影响。