Inconsistent relation of MAPK activation to infarct size reduction by ischemic preconditioning in pigs

被引:67
作者
Behrends, M
Schulz, R
Post, H
Alexandrov, A
Belosjorow, S
Michel, MC
Heusch, G
机构
[1] Univ Essen Gesamthsch Klinikum, Zentrum Innere Med, Abt Pathophysiol, D-45122 Essen, Germany
[2] Univ Essen Gesamthsch Klinikum, Zentrum Innere Med, Abt Nieren & Hochdruckkrankheiten, D-45122 Essen, Germany
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2000年 / 279卷 / 03期
关键词
p38; extracellular signal-regulated kinase; c-Jun NH2-terminal kinase; Western blot; myocardial ischemia-reperfusion;
D O I
10.1152/ajpheart.2000.279.3.H1111
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The importance of the activation of mitogen-activated protein kinases (MAPK) for the cardioprotection achieved by ischemic preconditioning (IP) is still controversial. We therefore measured infarct size and p38, extracellular signal-regulated kinase (ERK), and c-Jun NH2-terminal kinase (JNK) MAPK phosphorylation (by biopsies) in enflurane-anesthetized pigs. After 90 min low-flow ischemia and 120 min reperfusion, infarct size averaged 18.3 +/- 12.4 (SD)% (group 1, n = 14). At similar subendocardial blood flows, IP by 10 min ischemia and 15 min reperfusion (group 2, n = 14) reduced infarct size to 6.2 +/- 5.1% (P < 0.05). An inconsistent increase in p38, ERK, and p54 JNK phosphorylation (by Western blot) was found during IP; p46 JNK phosphorylation increased with the subsequent reperfusion. At 8 min of the sustained ischemia, p38, ERK, and p54 JNK phosphorylation were increased with no difference between groups (medians: p38: 207% of baseline in group 1 vs. 153% in group 2; ERK: 142 vs. 144%; p54 JNK: 171 vs. 155%, respectively). MAPK phosphorylation and reduction of infarct size by IP were not correlated, thus not supporting the concept of a causal role of MAPK in mediating cardioprotection by IP.
引用
收藏
页码:H1111 / H1119
页数:9
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