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Am J Physiol Heart Circ Physiol 279: H1111-H1119, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 3, H1111-H1119, September 2000

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

Matthias Behrends1, Rainer Schulz1, Heiner Post1, Alexander Alexandrov1, Sergej Belosjorow1, Martin C. Michel2, and Gerd Heusch1

1 Abteilung für Pathophysiologie, 2 Abteilung für Nieren- und Hochdruckkrankheiten, Zentrum für Innere Medizin des Universitätsklinikums Essen, 45122 Essen, Germany

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.

p38; extracellular signal-regulated kinase; c-Jun NH2-terminal kinase; Western blot; myocardial ischemia-reperfusion


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