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

用成年大鼠建立了失血性休克、内脏缺血性休克和肺损伤三种脏器损伤模型。这些方法以前曾报道过。以PBN为捕集剂，研究了自由基捕集的新技术。细节之前已经报道过了。用NSR光谱法定量分析PBN中自由基的含量，失血性休克2小时后，肝脏中自旋产物的产生增加到270%。在内脏动脉闭塞解除后，立即观察到肠道中的自旋分支前体的小而短暂的升高，随后降低至对照水平。在内脏缺血休克模型中，再灌注30分钟后，脊髓神经元的生成量明显增加，90分钟后达高峰。在肺损伤模型中，气管内注射黄嘌呤-黄嘌呤氧化酶溶液后，自由基产生呈线性增加。3种损伤动物脏器脂质过氧化反应均与氧自由基产生平行增加，休克动物应用别嘌呤醇、超氧化物歧化酶等氧自由基清除剂。Alopurinol对内脏缺血性休克和肺损伤模型无明显损伤作用，SOD对氧自由基的产生有抑制作用，而经氮芥处理后无白色血细胞的大鼠肠组织产生仍处于低水平，提示这些血细胞可能参与了组织损伤的产生。

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.