论文部分内容阅读
目的通过检测心跳骤停犬复苏后及给予纳洛酮干预后脑组织中一氧化氮(NO)、S100蛋白表达情况,了解纳洛酮对脑复苏的影响。方法18只健康杂种犬,随机分成三组,每组6只,予体外电击诱发室颤,对照组心跳骤停后予标准心肺复苏术;纳洛酮组心跳骤停后予标准心肺复苏术+纳洛酮;空白组不诱发室颤,于复苏后6h取脑海马组织行脑形态学检查及NO、S100蛋白表达的测定。结果纳洛酮组S100蛋白表达明显低于对照组(P<0.01),对照组脑组织NO的含量高于纳洛酮组(P<0.01),纳洛酮组脑组织的病理损害低于对照组。结论使用纳洛酮后心肺复苏犬脑组织的病理损害有所减轻,脑组织NO、S100蛋白的生成也显著减少,纳洛酮可能通过减少NO、S100蛋白的表达而减轻心肺复苏后脑的再灌注损伤。
Objective To investigate the effect of naloxone on cerebral resuscitation by detecting the expression of nitric oxide (NO) and S100 protein in brain tissue after cardioversion and after naloxone intervention. Methods Eighteen healthy mongrel dogs were randomly divided into three groups with 6 rats in each group, which were induced by extracorporeal shock in ventricular fibrillation. The control group was given standard cardiopulmonary resuscitation after a sudden cardiac arrest. The patients in naloxone group were treated with standard cardiopulmonary resuscitation Naloxone. The ventricular fibrillation was not induced in the blank group. The brain hippocampus was harvested at 6 hours after resuscitation for morphological examination and the expression of NO and S100 protein. Results The expression of S100 protein in naloxone group was significantly lower than that in control group (P <0.01). The content of NO in brain tissue in control group was higher than that in naloxone group (P <0.01) group. Conclusion Naloxone can attenuate the pathological changes of brain tissue after CPR and decrease the production of NO and S100 in brain tissues. Naloxone may reduce the reperfusion of brain after cardiopulmonary resuscitation by decreasing the expression of NO and S100 damage.