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在连接蛋白43缺陷小鼠中,后适应对心脏的保护作用未丧失。

No loss of cardioprotection by postconditioning in connexin 43-deficient mice.

作者信息

Heusch Gerd, Büchert Astrid, Feldhaus Sandra, Schulz Rainer

机构信息

Institut für Pathophysiologie, Zentrum für Innere Medizin Universitätsklinikum Essen, Hufelandstr. 55, 45122, Essen, Germany.

出版信息

Basic Res Cardiol. 2006 Jul;101(4):354-6. doi: 10.1007/s00395-006-0589-0. Epub 2006 Mar 27.

Abstract

In situ hearts and isolated cardiomyocytes from heterozygous connexin 43-deficient (Cx43+/-) mice cannot be protected by ischemic preconditioning or diazoxide. We have now addressed the role of connexin 43 in ischemic postconditioning (PC). Wild type (WT) and Cx43+/- mice were subjected to 30 min coronary occlusion and 120 min reperfusion, with and without a PC protocol of three cycles of 10 s coronary occlusion/10 s reperfusion. Infarct size (TTC staining) was reduced by PC from 54+/-5 to 37+/-3% of area at risk in WT. Likewise, infarct size was reduced by PC from 53+/-4 to 34+/-3% of area at risk in Cx43+/-. We conclude that connexin 43 is no prerequisite for PC's protection. To this end, the signal transduction of ischemic preconditioning and postconditioning differs.

摘要

来自杂合性连接蛋白43缺陷(Cx43+/-)小鼠的原位心脏和分离的心肌细胞不能受到缺血预处理或二氮嗪的保护。我们现在研究了连接蛋白43在缺血后处理(PC)中的作用。野生型(WT)和Cx43+/-小鼠接受30分钟冠状动脉闭塞和120分钟再灌注,有或没有10秒冠状动脉闭塞/10秒再灌注的三个周期的PC方案。在WT中,PC使梗死面积(TTC染色)从危险区域面积的54±5%减少到37±3%。同样,在Cx43+/-中,PC使梗死面积从危险区域面积的53±4%减少到34±3%。我们得出结论,连接蛋白43不是PC发挥保护作用的先决条件。为此,缺血预处理和后处理的信号转导是不同的。

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