缺血后适应对兔楔形心肌块模型再灌注室性心律失常的影响

发布时间：2018-10-07 19:13

【摘要】：【目的】缺血后适应作为一种新的冠心病介入治疗措施，，在预防缺血再灌注损伤、降低心肌梗死面积中起着重要作用。本实验旨在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，并在实验中测定相关的电生理参数和缝隙连接蛋白受缺血后适应的影响情况，探讨缺血后适应维持电生理稳定性的可能机制。【方法】将家兔随机分为正常对照组、缺血再灌注组和缺血后适应组。缺血再灌注组合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，回复台氏液灌注2h。记录心肌块内、外膜心肌细胞跨壁动作电位、跨壁心电图，并测量有效不应期，室性心律失常诱发率等电生理参数。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Cx43（NP-Cx43）。【结果】在建立好的楔形心肌块模型中观察到：①对照组、缺血再灌注组、缺血后适应组的室性心动过速（VT）诱发率分别是0/10,8/10,1/10，缺血再灌注组与缺血后适应组VT发生率比对照组显著增高（P0.05），缺血后适应组与缺血再灌注组相比VT发生率明显降低（P0.05）。②与缺血再灌注组相比，缺血后适应组的跨室壁离散度（TDR）、有效不应期（ERP）等电生理参数得到改善，差异有统计学意义（P0.05）。利用免疫荧光法检测心肌组织中的缝隙连接蛋白，发现对照组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，经过相对灰度比较差异有统计学意义（P0.05）。【结论】缺血后适应可以改善建立好的楔形心肌块缺血再灌注模型室性心率失常诱发率，并可以改善心肌块缺血再灌注后的多种电生理参数，同时改善缺血心肌组织中缝隙连接蛋白重构。降低缺血心肌组织中缝隙连接蛋白去磷酸化可能是缺血后适应维持心脏电生理稳定的机制之一。
[Abstract]:[objective] as a new interventional therapy for coronary heart disease, adaptation after ischemia plays an important role in preventing ischemia reperfusion injury and reducing myocardial infarction area. The purpose of this study was to observe the effect of ischemic adaptation on ventricular arrhythmias induced by ischemia reperfusion in rabbit left ventricular wedge block, and to determine the relative electrophysiological parameters and gap junction protein (CGN). To explore the possible mechanism of adaptation to maintain electrophysiological stability after ischemia. [methods] Rabbits were randomly divided into normal control group, ischemia reperfusion group and ischemic adaptation group. After ischemia reperfusion combined with ischemia adaptation group, the wedge myocardial block model was established for 1 hour, and the Tetranyl fluid perfusion was stopped for 45 min. The ischemia reperfusion group continued to perfuse Tetranys fluid for 2 h. The adaptation group was treated with 10 S reperfusion at the beginning of reperfusion, and 10s was stopped after reperfusion. After repeated 6 times, the solution was perfused for 2 h. Transmural action potential, transmural electrocardiogram, effective refractory period and ventricular arrhythmia evoked rate were recorded. The dephosphorylation gap junction protein Cx43 (NP-Cx43) was detected by immunofluorescence. [results] in the established wedge myocardial mass model, the control group of 1: 1, the ischemia-reperfusion group, were observed. The (VT) evoked rate of ventricular tachycardia in ischemic adaptation group was 0 / 108 / 10 / 10 respectively. The incidence of VT in ischemia reperfusion group and adaptation group was significantly higher than that in control group (P0.05). The incidence of VT in ischemic adaptation group was significantly lower than that in ischemia reperfusion group (P0.05). (P0.05) compared with the ischemia-reperfusion group, The electrophysiological parameters such as (ERP) in the effective refractory period of transventricular dispersion (TDR),) were improved in the adaptation group after ischemia (P0.05). Using immunofluorescence assay to detect gap junction protein in myocardial tissue, it was found that the distribution of NP-Cx43 in the control group was very small, and the content of NP-Cx43 in the ischemia reperfusion group was increased and distributed mostly at the end and end junctions of myocardial cells. The content of NP-Cx43 in the adaptation group after ischemia was significantly lower than that in the ischemia-reperfusion group, and the difference was statistically significant (P0.05). [conclusion] adaptation after ischemia can improve the induced rate of ventricular arrhythmias in a wedge myocardial ischemia reperfusion model, and can improve the electrophysiological parameters of myocardial ischemia reperfusion. At the same time, the gap junction protein remodeling in ischemic myocardium was improved. Decreasing gap junction protein dephosphorylation in ischemic myocardium may be one of the mechanisms of adaptation to maintain cardiac electrophysiological stability after ischemia.
【学位授予单位】：华中科技大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R541.4;R-332

【相似文献】