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

不同类型休克动物内脏器官氧自由基产生的定量

基本信息

批准号：
04670942
负责人：
OGAWA Ryo
金额：
$ 1.28万
依托单位：
Nippon Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

项目摘要

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.

以成年大鼠为对象制作休克致器官损伤（出血性、内脏缺血性和肺损伤）三种模型。这些方法之前已报道过。采用PBN作为捕获剂捕获自由基的新技术。详细情况之前已报道过。使用 NSR 光谱法对 PBN 中捕获的自由基进行定量分析。失血性休克 2 小时后，肝脏中自旋产物的产生增加至 270%。在内脏动脉闭塞解除后立即观察到肠道中自旋导管产生的小幅暂时升高，随后降低至对照水平。在内脏缺血休克模型中，再灌注后 30 分钟后，自旋产物的产生显着增加，并在 90 分钟后达到峰值。在肺损伤模型中，将黄嘌呤-黄嘌呤氧化酶溶液注射入气管后，自由基产生线性升高。 3种损伤动物器官中脂质过氧化作用与氧自由基产生呈平行增加。对休克动物给予别嘌呤醇、超氧化物歧化酶等氧自由基清除剂。阿洛嘌呤醇没有表现出任何有效的损伤，超氧化物歧化酶在内脏缺血休克和肺损伤模型中表现出抑制氧自由基产生的作用。在通过氮马斯塔菠导管预处理而没有白细胞的大鼠中，肠的产生仍然处于较低水平状态，表明这些血细胞在组织损伤的产生中可能发挥作用。