Iwai A, Itoh M, Yokoyama Y, Yasue N, Miyamoto T, Joh T, Matsusako K, Endoh K, Kawai T, Takeuchi T
First Department of Internal Medicine, Nagoya City University Medical School Japan.
Scand J Gastroenterol Suppl. 1989;162:63-6. doi: 10.3109/00365528909091126.
Ischemia-reperfusion induced extensive gastric mucosal injury and an increase in chemiluminescence activity of neutrophils obtained from the portal vein in hemorrhagic shock rats. CV-3988, a selective antagonist of platelet activating factor (PAF), significantly reduced the gross and histologic gastric damage, and the increase in chemiluminescence activity of neutrophils. These results suggest that PAF generated on hypoxia might stimulate oxygen radical production by neutrophils, resulting in the occurrence of gastric injury in hemorrhagic shock rats.
缺血再灌注可导致失血性休克大鼠广泛的胃黏膜损伤,并使门静脉中性粒细胞的化学发光活性增强。血小板活化因子(PAF)的选择性拮抗剂CV-3988可显著减轻胃的大体和组织学损伤,以及中性粒细胞化学发光活性的增强。这些结果表明,缺氧时产生的PAF可能刺激中性粒细胞产生氧自由基,从而导致失血性休克大鼠发生胃损伤。