No loss of cardioprotection by postconditioning in connexin 43-deficient mice
No loss of cardioprotection by postconditioning in connexin 43-deficient mice
复制标题
DOI：
10.1007/s00395-006-0589-0
复制
发表时间：
2006-07-01
影响因子：
9.5
通讯作者：
Schulz, R
中科院分区：
文献类型：
--
作者：
Heusch, G;Büchert, A;Schulz, R
来自杂合子连接蛋白43缺陷（Cx43（+/-））小鼠的原位心脏和分离的心肌细胞不能被缺血预处理或二氮嗪保护。我们现在讨论了连接蛋白43在缺血后处理（PC）中的作用。将野生型（WT）和Cx43（+/）小鼠进行30 min冠状动脉闭塞和120 min再灌注，有和没有10 s冠状动脉闭塞/10 s再灌注的三个循环的PC方案。通过PC，CT大小（TTC染色）从WT中风险面积的54 +/- 5降至37 +/- 3%。同样，PC使Cx43（+/-）危险区域的梗死面积从53 +/- 4减少到34 +/- 3%。我们的结论是，连接蛋白43不是PC的保护的先决条件。为此，缺血预适应和后适应的信号转导不同。
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.