摘要
目的 :研究缺血预处理的心肌保护作用 ,并对其机制进行初步探讨。方法 :采用Langendorff离体心脏灌流法 ,2 4只鼠心随机分成对照、单纯缺血、缺血预处理、纳络酮处理等 4组。于复灌后 1 0 min记录心脏功能指标和冠状动脉流出液中的心肌肌酸激酶 ( CK)含量。结果 :经过缺血预处理 ,持续缺血后冠状动脉流出液中肌酸激酶含量明显下降 ,心肌收缩功能也有明显改善 ,而灌注液中加入纳络酮 ( NAL)使缺血预处理的心肌保护作用消失。结论 :在鼠心离体工作模型中经过 2个循环的 5 min缺血和 5 min再灌注即可诱导鼠心的缺血预处理作用 ,此种作用并可被非特异性阿片受体拮抗剂纳络酮所阻断 。
Objective:To observe the salutary effects of ischemic preconditioning (IPC) on heart after global ischemia/reperfusion (GI/R) and discover the potential mechanism of this phenomenon. Methods:The adult mice hearts were perfused in Langendorff mode. 24 hearts were randomly divided into four groups: Control Group,Ischemic Group,IPC Group,NAL+IPC Group. Hemodynamic parameters and CK release were observed in the 10th after reperfusion. Results:Following sustained GI/R, in IPC Group, CK release was significantly reduced and Hemodynamic parameters were better. Naloxone infusion blocked the protection from IPC in isolated hearts including CK release. Conclusion:In the isolated mouse heart,two cycles of IPC with 5 min ischemia and 5 min reperfusion are necessary to induce the cardioprotection in the mouse heart, which can be blocked by the naloxone infusion, The cardioprotection induced by IPC is associated with opioid receptor.
出处
《吉林大学学报(医学版)》
CAS
CSCD
北大核心
2003年第4期465-467,共3页
Journal of Jilin University:Medicine Edition
关键词
缺血预处理
心肌
心肌再灌注损伤
受体
阿片样
Ischemic preconditioning,myocardial
Myocardial reperfusion injury
Receptors,opioid