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

被引：116

作者：

Heusch, G ^{[1
]}

Büchert, A ^{[1
]}

Feldhaus, S ^{[1
]}

Schulz, R ^{[1
]}

机构：

[1] Univ Klinikum Essen, Zentrum Innere Med, Inst Pathophysiol, D-45122 Essen, Germany

来源：

BASIC RESEARCH IN CARDIOLOGY | 2006年 / 101卷 / 04期

关键词：

myocardial ischemia; reperfusion; signal transduction; ischemic postconditioning; myocardial infarction;

D O I：

10.1007/s00395-006-0589-0

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：354 / 356

页数：3

共 18 条

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