Maeda Y
First Department of Surgery, Yamanashi Medical College.
Nihon Shokakibyo Gakkai Zasshi. 1990 Jul;87(7):1483-90.
Acute gastric mucosal lesion (AGML) was induced six hours after the administration of endotoxin. The decrease of gastric mucosal blood flow, used to be supposed as an important factor of the formation of AGML, was not found, but thiobarbituric acid (TBA) reactants in the gastric mucosa were increased three hours after endotoxin injection, 198 +/- 18.2 (vs control 130 +/- 18.2). The administration of platelet activating factor (PAF) inhibitor, CV3988, reduced the formation of AGML and increase of the TBA reactants. These results suggested that the chemical mediator like PAF and free radicals may play an important role in the pathogenesis of gastric mucosal injury induced by endotoxemia, without the decrease of mucosal blood flow.
内毒素给药6小时后诱发急性胃黏膜病变（AGML）。过去曾认为胃黏膜血流量减少是AGML形成的一个重要因素，但未发现这种情况，不过内毒素注射3小时后胃黏膜中的硫代巴比妥酸（TBA）反应物增加，为198±18.2（对照组为130±18.2）。给予血小板活化因子（PAF）抑制剂CV3988可减少AGML的形成及TBA反应物的增加。这些结果表明，像PAF和自由基这样的化学介质可能在内毒素血症诱导的胃黏膜损伤发病机制中起重要作用，而不伴有黏膜血流量的减少。
