Piqué J M, Pérez Ayuso R M, Bilbao J, Terés J
Gastroenterology Department, Hospital Clinic, University of Barcelona, Spain.
Dig Dis Sci. 1991 Dec;36(12):1715-20. doi: 10.1007/BF01296615.
Intravenous administration of platelet-activating factor (PAF) induces extensive damage in rat gastric mucosa. The aim of the present study was to examine whether the presence or absence of acid in the gastric lumen could modify the PAF-induced gastric damage. The effects of inhibition of basal and pentagastrin-stimulated acid secretion by ranitidine on the deep histological gastric damage induced by 30 min of infusion of PAF (100 ng/kg/min) were assessed by using a histological score. Inhibition of basal gastric acid secretion did not prevent the histological gastric damage induced by PAF. Stimulation of gastric acid secretion by pentagastrin significantly increased PAF-induced gastric damage, and this effect was reversed by a dose of ranitidine that returns acid secretion to baseline levels. This acid-related damage was confined to the deep mucosa, since scanning electron microscope analysis ruled out an additional surface damage in PAF-infused rats when gastric acid was stimulated. The data indicate that a certain amount of acid may worsen the deep gastric mucosal damage induced by PAF.
静脉注射血小板活化因子（PAF）可导致大鼠胃黏膜广泛损伤。本研究的目的是探讨胃腔内酸的存在与否是否会改变PAF诱导的胃损伤。通过组织学评分评估雷尼替丁对基础胃酸分泌和五肽胃泌素刺激的胃酸分泌的抑制作用对输注PAF（100 ng/kg/分钟）30分钟所诱导的深度组织学胃损伤的影响。抑制基础胃酸分泌并不能预防PAF诱导的组织学胃损伤。五肽胃泌素刺激胃酸分泌显著增加了PAF诱导的胃损伤，而一剂使胃酸分泌恢复到基线水平的雷尼替丁可逆转这种效应。这种与酸相关的损伤局限于深层黏膜，因为扫描电子显微镜分析排除了胃酸受刺激时PAF输注大鼠的额外表面损伤。数据表明，一定量的酸可能会加重PAF诱导的深层胃黏膜损伤。
