失血性休克复合氰化钠中毒对兔心肌功能的影响  

Effects of hemorrhagic shock and sodium cyanide intoxication on function of the rabbit′s cardiac muscle

作　　者：朱乐明[1] 董兆君[2] 

机构地区：[1]南京军区疾病预防控制中心,南京医学硕士210002 [2]第三军医大学军事预防医学院防化医学教研室,重庆400038

出　　处：《医学研究生学报》2010年第5期460-464,共5页Journal of Medical Postgraduates

基　　金：全军医学卫生科研基金(06G077)

摘　　要：目的失血性休克合并化学毒剂中毒在化学毒剂复合伤中所占比例较大,目前尚无成熟的救治方案。探讨氰化钠(sodium cyanide,NaCN)中毒和失血性休克这2种致伤因素对心肌功能的影响,为研究适合于化学毒剂伤复合失血性休克的救治方案,提高化学毒剂复合伤的救治水平提供依据。方法建立NaCN中毒复合失血性休克模型,观察心电、血压、心肌酶谱等心血管功能变化情况,研究失血性休克条件下NaCN的毒性作用特点。结果 NaCN中毒复合失血性休克后心电图Q-T间期明显延长,心肌酶学指标显著升高。结论失血性休克条件下,NaCN毒性明显增加;心肌复极过程紊乱,心肌酶含量显著增加,提示心肌细胞损伤。NaCN与失血性休克可能通过相同的作用机制,引起心肌细胞的损伤,对机体造成更严重的损害。Objective To determine the influences of hemorrhagic shock and cyanide intoxication on the injuries of the function of cardiac muscles.Methods Combined injury animal models were established in rabbits.The function of respiration and circulation were recorded with electrophysiological system.Myocardial enzymes were analyzed biochemically.Results There was an extension in Q-T stage when cardiac function was damaged by heorrhagic shock and cyanide intoxication.Myocardial enzymes were changed significantly.Conclusion Hemorrhage shock elevated the toxicity of sodium cyanide.Disorder in the course of cardiac muscle repolarization and obvious increasement in the amount of cardiac muscle enzymes can cause damage to cardiocytes.

关 键 词：失血性休克 氰化钠 毒性 心肌功能 

分 类 号：R364.14[医药卫生—病理学]