Quantitation of oxygen radaical production of splanchnic organs in animals with various types of shock

以成年大鼠为实验对象，建立了出血性、内脏缺血和肺损伤三种器官损伤模型。这些方法已在前面报道过。采用PBN捕集剂捕获自由基的新技术。细节之前已经报道过了。用NSR光谱法定量分析了PBN中的自由基。失血性休克2小时后，肝内旋成体的生成增加到270%。在释放内脏动脉闭塞后，观察到肠内自旋成体的产生短暂而小的升高，随后降低到控制水平。在内脏缺血休克模型中，自旋成体的产生在再灌注后30分钟显著增加，并在再灌注后90分钟达到峰值。肺损伤模型经气管注射黄嘌呤-黄嘌呤氧化酶溶液后，自由基生成呈线性升高。三种损伤动物的器官中脂质过氧化作用与氧自由基的产生平行增加。氧自由基清除剂如别嘌呤醇和超氧化物歧化酶应用于休克动物。在内脏缺血、休克和肺损伤模型中，Alopurinol对氧自由基的产生没有明显的抑制作用，而超氧化物歧化酶对氧自由基的产生有抑制作用。在没有白细胞的大鼠中，通过预处理氮mastard spinad成人肠道的生产仍然处于低状态，这表明这些血细胞可能在组织损伤的生产中起作用。

Three models of organ injury induced by shock (hemorrhagic, splanchnic ischemia and lung injury) were made on adult rats. The methods were reported previously. New techniques were emplyed for trapping of radicals using PBN as a trapper. The details were reprted previously. Radaicals trapped into PBN were analyzed quantitatively using NSR spectrometry.Spin aducts production in liver was increased to 270% after 2 hour of hemorrhagic shock. A small and tempoary elevation of spin aducts prodeuction in bowels was observed immediately after release of splanchinic artery occlusion, followed by reduction to control levels. Spin aducts production increased markedly after 30 minutes after reperfusion and show a peak at 90 minutes after in splanchnic ischemia shock model. On lung injury model radical production elevated linearly after injection of xanthine-xanthine oxidase solution into trachea. Lipid peroxidation increased pararelly to production of oxygen free radaicals in organ of animals subjected to 3 types of injury.Oxygen radical scavengers such as allopurinol and superoxide dismutase were applied on animals with shock. Alopurinol did not show any effective insults, Superoxide dismutase showed a suppressive effect of oxygen radical production in splanchnic ischemia shock and lung injury models.In rats which have no white blood corpuscle by pre-treatment of nitrogen mastard spinaducts production of bowel remained in a low state, suggesting a possible role of these blood cells in produciton of tissue injuries.