论文部分内容阅读
为了探讨创伤性休克时脏器一氧化氮合酶 (NOS)的动态变化及NOS抑制剂、L 精氨酸对创伤性休克的治疗效果 ,作者复制了大鼠创伤性休克模型 ,检测创伤性休克后 0 5h、3h、5h心脏、肺脏、小肠、肝脏、脾脏中iNOS和cNOS的变化 ;另外在休克后静脉予氨基胍(AG)、左旋硝基精氨酸甲酯(L NAME)、左旋精氨酸 (L Arg) ,检测大鼠脏器中iNOS和cNOS的变化 ,观察在给药后动物的生存时间和死亡率。结果表明 ,正常大鼠所有脏器均有cNOS表达 ,肝脏和肺脏还有少量iNOS分布。创伤性休克后 0 5h几乎所有脏器cNOS有不同程度的提高 ,而iNOS却无明显变化 ;休克后 3h,脏器中cNOS开始下降 ,而iNOS开始上升 ,到休克后 5h ,iNOS大量合成 ,与对照组比较差异显著 (P <0 0 1)。AG和L Arg明显延长了休克大鼠的生存时间 ,而L NAME对生存率无影响。AG抑制了iNOS的合成 ,同时促进了cNOS的合成 ,L NAME对两种NOS均抑制 ,而L Arg对NOS没有影响。结果提示 ,iNOS在创伤性休克后期才大量合成 ,应用NOS抑制剂和L Arg治疗休克必须视休克的程度、药物的剂量和给药时机而定。
To investigate the dynamic changes of nitric oxide synthase (NOS) and the therapeutic effect of NOS inhibitor and L-arginine on traumatic shock in traumatic shock, the authors copied the traumatic shock model of rats to detect traumatic shock The changes of iNOS and cNOS in heart, lung, small intestine, liver and spleen at 0h, 3h, 5h were observed. In addition, AG, L NAME, (L Arg). The changes of iNOS and cNOS in the visceral organs of rats were observed. The survival time and mortality of the animals were observed after administration. The results showed that cNOS expression was observed in all organs of normal rats, with a small amount of iNOS distribution in liver and lung. At 0h after traumatic shock, cNOS in all organs increased to some extent, but iNOS showed no significant change. After 3h after shock, cNOS began to decline in organ and iNOS began to rise. After 5h of shock, iNOS was synthesized in a large amount, The difference between the control group was significant (P <0.01). AG and L Arg significantly prolonged survival in shock rats, while L NAME had no effect on survival. AG inhibited the synthesis of iNOS and promoted the synthesis of cNOS. L NAME inhibited both NOS and L Arg had no effect on NOS. The results suggest that iNOS is synthesized only after the late stage of traumatic shock. The treatment of shock with NOS inhibitors and L Arg must depend on the degree of shock, the dosage of the drug and the timing of administration.