Fukuoka S, Urakawa T, Saitoh Y
Nihon Geka Gakkai Zasshi. 1987 Jun;88(6):701-9.
Changes in gastric mucosal blood flow in acute gastric ulceration associated with hemorrhagic shock were investigated for their relationship to gastric mucosal PGE2 and NA in rats which were deprived of 24 ml/kg of blood. The results were: 1. Gastric mucosal blood flow and NA were decreased by 65% and 25% respectively at 30 minutes after hemorrhage. Gastric mucosal PGE2 was 26% increased at 30 minutes after exsanguination and then showed a marked decrease. 2. Administration of NA resulted in an 100% increase of gastric mucosal PGE2. However, animals receiving NA at 20 or 50 minutes after hemorrhage gave values for gastric mucosal PGE2 which were not different from those of non-NA-treated animals at 30 and 60 minutes after hemorrhage. 3. Pre-treatment with PGE2 suppressed the reduction in both gastric mucosal blood flow and NA and the development of ulcer, whereas pre-treatment with indomethacin accelerated them. These results suggest that the increase in gastric mucosal PGE2 in early shock might represent a phenomenon of adaptation to decreased blood flow, implicating adrenergic activation as one of causative factors, and the decrease in gastric mucosal PGE2 in late shock might be construed as the result of impaired synthesis of PGE2 due to persistent hypoxia and be one of the possible factors for ulcers.
研究了失血性休克相关的急性胃溃疡大鼠胃黏膜血流量变化与胃黏膜前列腺素E2（PGE2）和去甲肾上腺素（NA）的关系，这些大鼠失血24 ml/kg。结果如下：1. 出血后30分钟，胃黏膜血流量和NA分别下降65%和25%。放血后30分钟，胃黏膜PGE2增加26%，随后显著下降。2. 给予NA导致胃黏膜PGE2增加100%。然而，在出血后20或50分钟接受NA的动物，其胃黏膜PGE2值与出血后30和60分钟未接受NA治疗的动物无差异。3. 用PGE2预处理可抑制胃黏膜血流量和NA的减少以及溃疡的发生，而用吲哚美辛预处理则加速这些变化。这些结果表明，休克早期胃黏膜PGE2的增加可能代表对血流量减少的一种适应现象，提示肾上腺素能激活是致病因素之一，而休克晚期胃黏膜PGE2的减少可能被解释为由于持续缺氧导致PGE2合成受损的结果，并且是溃疡发生的可能因素之一。
