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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Preconditioning in the absence or presence of sustained ischemia modulates myocardial Cx43 protein levels and gap junction distribution.
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Preconditioning in the absence or presence of sustained ischemia modulates myocardial Cx43 protein levels and gap junction distribution.

机译:在不存在或存在持续性缺血的情况下进行预处理可调节心肌Cx43蛋白水平和间隙连接分布。

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摘要

In the heart, brief repeated episodes of ischemia prior to a sustained occlusion (ischemic preconditioning; PC) significantly delay the onset of necrosis and arrhythmogenesis. Ischemia has been reported to influence gap junction organization and connexin43 (Cx43) content, but whether PC affects these structures is not known. We investigated the effect of PC (2 cycles of 5-min ischemia plus 10-min reperfusion) followed by prolonged reperfusion without concomitant regional coronary occlusion on the myocardial Cx43 content and its spatial distribution in rabbit hearts. We also compared the effect of sustained ischemia with or without PC on Cx43 spatial distribution. In experiments with PC only, there was an initial decrease in Cx43 levels within the ischemic zone followed by a progressive increase after 48 h reperfusion. End-to-end immunolabeling of Cx43 was augmented in the ischemic region between 24 and 48 h reperfusion; labeling was not uniquely confined to myocyte abutments, but was also dispersed along the sarcolemma. Cx43 immunolabelling was more intense and diffuse in hearts subjected to PC before sustained coronary occlusion (compared to non-PC). These data indicate that gap junctions are significantly altered during brief episodes of ischemia. Reorganization of the gap junction complex could contribute to PC-mediated reductions in cardiac arrhythmias.
机译:在心脏中,持续性闭塞(缺血预处理; PC)之前短暂的反复缺血发作显着延迟了坏死和心律失常的发生。据报道,缺血会影响间隙连接组织和连接蛋白43(Cx43)的含量,但尚不清楚PC是否影响这些结构。我们研究了PC(2个周期的5分钟局部缺血再加上10分钟再灌注),然后进行长时间再灌注而不伴随局部冠状动脉闭塞对兔心脏心肌Cx43含量及其空间分布的影响。我们还比较了有或无PC的持续缺血对Cx43空间分布的影响。在仅使用PC的实验中,缺血区域内Cx43的水平开始下降,然后再灌注48 h后逐渐上升。 Cx43的端到端免疫标记在24至48 h再灌注之间的缺血区域增加;标记不仅限于肌细胞基台,而且还沿肌膜分散。 Cx43免疫标记在持续冠状动脉闭塞之前(与非PC相比)在接受PC的心脏中更为强烈和弥漫。这些数据表明,在短暂的缺血发作期间,间隙连接明显改变。间隙连接复合体的重组可能有助于PC介导的心律失常的减少。

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