摘要
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。
In order to investigate the dynamic changes in nitric oxide synthase (NOS) activity in organs during traumatic shock and to evaluate the effects of inhibitor of NOS and L Arginine (L Arg) on traumatic shock, rat model of traumatic shock was established, and the constitutive NOS and inducible NOS in the heart, small intestine, liver, lung , spleen were measured 0 5h, 3h, 5h after traumatic shock. Followed by intravenous injection with aminoguanidine (AG ), N G nitro L arginine methyl ester (L NAME), or L Arg, NOS were again measured, and the survival time and 24h survival rate were recorded. It was found that in normal rats cNOS was expressed in all organs, but only a weak iNOS expression in lung and liver. Half an hour after shock, cNOS was elevated in almost all organs in various degrees but there was no change in iNOS. 3h after shock, an increase in iNOS activity and a decrease in cNOS were observed. The iNOS was synthesized in large quantity 5h after shock. AG and L Arg markedly prolonged the survival time but L NAME did not in shock rats. AG inhibited the activity of iNOS but promoted the synthesis of cNOS, and both NOS were inhibited in L NAME group, but not in L Arg group. The results that iNOS was synthesized in large quantity only at later period of traumatic shock. To treat shock, the inhibitors of NOS and L Arg should be given according to the degree of shock, the dosage of drugs, and the time of administration
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2003年第8期684-686,共3页
Medical Journal of Chinese People's Liberation Army
基金
广东省自然科学基金资助课题 (编号 0 0 1 0 4 8)
