缺血后适应对兔楔形心肌块缺血再灌注模型室性心律失常的影响

目的:观察缺血后适应对家兔左室楔形心肌块缺血再灌注模型室性心律失常诱发率的影响,并探讨其维持电生理稳定的机制。方法:将30只家兔随机分为对照组、缺血再灌注组和缺血后适应组,每组10只。缺血再灌注组和缺血后适应组在建立好楔形心肌块模型稳定1h后,停止台氏液灌注45min,缺血再灌注组继续灌注台氏液2h;缺血后适应组复灌初期采用复灌10s、停灌10s方案,重复6次后,恢复台氏液灌注2h。记录心肌块内、外膜心肌细胞跨壁动作电位、跨壁心电图、有效不应期(ERP)等电生理参数以及室性心律失常诱发率。实验结束后利用免疫荧光方法检测去磷酸化缝隙连接蛋白43(NP-Cx43)。结果:①对照组、缺血再灌注组、缺血后适应组的室性心动过速(VT)诱发率分别为0、80%(8/10)、10%(1/10),两两比较均差异有统计学意义(均P<0.05)。②与缺血再灌注组比较,缺血后适应组的跨室壁离散度、ERP等电生理参数得到改善,均差异有统计学意义(均P<0.05)。③免疫荧光显示对照组心肌NP-Cx43分布量极少;缺血再灌注组NP-Cx43含量增加且多分布在心肌细胞端端连接处;缺血后适应组NP-Cx43与缺血再灌注组相比含量要明显减少,差异有统计学意义(P<0.05)。结论:缺血后适应可显著降低室性心律失常诱发率,改善缝隙连接蛋白重构可能是其维持心脏电生理稳定的机制之一。

Effect of ischemic postconditioning on reperfusion induced ventricular arrhythmias in rabbit wedge preparation ischemia-reperfusion model

Objective:To observe the effect of ischemia-postconditioning on reperfusion induced ventricular arrhythmias in ischemia-reperfusion rabbit hearts and study the anti-arrhythmic mechanism of postconditioning.Method:Thirty rabbits were randomly divided into control group,ischemia group and ischemia-postconditioning group.All rabbits’ hearts were made into ventricular wedge preparations.In control group,preparations were perfused by tyrode’s solution,in ischemia group and ischemia-postconditioning group the tyrode’s solution were stopped perfusing for 45 min,then in the ischemia group still reperfused by tyrode’s solution;but in the ischemia-postconditioning group got the 6 times experience of 10 seconds transient ischemia at the beginning of reperfusion.Result:①The incidences of reperfusion arrhythmia in the 3 groups were 0,80%,10%,and there were significant differences among the 3 groups(P<0.05).②The electrophysiological parameters such as TDR,QT interval were improved in ischemia-postconditioning group compared with ischemia-reperfusion group(P<0.05).③Immunofluorescence results showed that there was a little NP-Cx43 distribution in control group,a certain amount of NP-Cx43 distribution in ischemia-postconditioning group,but it is fewer compared with the ischemia-group.All the NP-Cx43 centralized in the intercalated discs of cell.Conclusion:Ischemia-postconditioning prevents ventricular arrhythmia induced by ischemia-reperfusion,improving the gap junction restructure may be one of the principles.