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作 者:王悦喜[1] 董莉[1] 陈运贞[1] 刘元生[1]
机构地区:[1]重庆医科大学临床学院心血管内科,400016
出 处:《重庆医科大学学报》2000年第3期268-269,共2页Journal of Chongqing Medical University
摘 要:目的 探讨心肌缺血预处理(IPC)保护该心肌被以后较长时间缺血损伤的作用。方法 给Wistar大鼠在90min缺血和180min再灌注(I/R)前3次、每次5min、间隔5min再灌注的心肌缺血预处理;I/R前静脉注射Bre.、PMA观察它们对心肌I/R损伤的影响作用。结果 IPC、PMA可保护心肌被I/R的损伤;Bre.则可消除IPC对心肌的保护作用。结论 IPC可保护心肌被长达90min.I/180min.R损伤,其保护机制作者正在研究之中,可能与蛋白激酶C被激活有关。Objective To explore IPC(ischemic preconditioning) and PMA reduce the size of infarcts compared with control and breviscapini(Bre.). Methods and Results Anesthetized open-chest wistar rats underwent three 5- minute episodes of preconditioning ischemia in IPC group or after administration of Bre. in Bre.group; Control group had no episodes of ischemic preconditioning; PMA was injected 5 minutes before sustained occlusion; Afte- r 90 minutes of CAO and 3 hours of reperfusion, infarct size was significantly reduced in IPC rats' compared with control group and Bre.+IPC groups, P<0.01. Conclusion The wistar rats IPC model was stable, TTC can obviously distinguish the AN(area of necrosis) from normal myocardium. The IPC、PMA protected the myocardium from sustained ischemia-reperfusion injury.Bre. blunted the protective role of IPC. PMA imitated the protective role of IPC. Their protective mechanism will be disscused in detail in next article.
分 类 号:R542.2[医药卫生—心血管疾病]
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