休克发病机制与实验治疗的研究——小肠缺血在休克发病学中的作用

RESEARCH ON PATHOGENETIC MECHANISM AND EXPERIMENTAL THERAPY OF SHOCK——EFFECT OF INTESTINAL ISCHEMIA ON THE PATHOGENESIS OF SHOCK

休克过程的一个重要特点是:当它发展到一定阶段后,尽管针对病因和发病环节进行了积极治疗,过程仍循恶性循环进行性地加重以至死亡。关于休克的这种不可逆机制目前还不清楚,许多学者注意到休克时缺血的腹腔内脏对休克不可逆发展有特别重要的意义。我们利用肠系膜上动脉闭塞性休克（Superior mesenteric artery occlusion shock,简称SMAO休克）模型,以H2O2,654-2,POB作实验性治疗,对小肠缺血在休克发病学中的作用进行探讨并分析了654-2抗休克的机理,结果报告如下。

Superior mesenteric artery occlusion (SMAO)shock was reproduced in rabbits under local anesthesia as shock model. It Was shown that primary intestinal ischemic damage itself could lead to severe irreversible shock. Further experiments demonstrated that antegrade intraarterial infusion of H_2O_2 IE, or Ⅳ medication of Anisodamine had improved intestinal tissue ischemia, and prevented the irreversibility of the shock process. These results suggested that small intestine is probably the "key organ" in the occurrence of irreversible shock.654-2 given intraenterically decreased the release of lysozymal enzyme (acid phosphatase) from the ischemic intestine, which tissue was obviously protected, and shock could be relieved, while α-adrenergic blocking agent phenoxybenzamine showed no antishock effect in our experimens