Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580
Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580
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DOI：
10.1152/ajpheart.01183.2004
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发表时间：
2005-06-01
影响因子：
4.8
通讯作者：
Imamura, H
中科院分区：
文献类型：
--
作者：
Sumida, T;Otani, H;Imamura, H
P38 MAPK的激活不仅对线粒体有害，而且对收缩功能也是有害的。因此，p38MAPK抑制治疗是预防心脏再灌注损伤的一种有前途的方法。然而，逆转p38MAPK介导的收缩功能障碍可能会破坏缺血再灌流心肌细胞脆弱的肌膜。因此，我们假设，当收缩功能同时被阻断时，再灌流期间抑制p38 MAPK的有益效果可以增强。分离和灌流的大鼠心脏以330转/分的速度起搏，然后进行20分钟的缺血再灌流。P38MAPK在缺血后和再灌流早期即被激活(
p38 MAP kinase activation is known to be deleterious not only to mitochondria but also to contractile function. Therefore, p38 MAP kinase inhibition therapy represents a promising approach in preventing reperfusion injury in the heart. However, reversal of p38 MAP kinase-mediated contractile dysfunction may disrupt the fragile sarcolemma of ischemic-reperfused myocytes. We, therefore, hypothesized that the beneficial effect of p38 MAP kinase inhibition during reperfusion can be enhanced when contractility is simultaneously blocked. Isolated and perfused rat hearts were paced at 330 rpm and subjected to 20 min of ischemia followed by reperfusion. p38 MAP kinase was activated after ischemia and early during reperfusion (