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in
cardiomyocytes
Department of Anesthesiology, University of North Carolina, Chapel Hill, North Carolina 27599
Oxygen
radicals and protein kinase C (PKC) mediate ischemic
preconditioning. Using a cultured chick embryonic cardiomyocyte model
of hypoxia and reoxygenation, we found that the oxygen radicals generated by ischemic preconditioning were
H2O2. Like preconditioning, H2O2 selectively activated the 
-isoform of
PKC in the particulate compartment and increased cell viability after
1 h of hypoxia and 3 h of reoxygenation. The glutathione
peroxidase ebselen (converting H2O2 to
H2O) and the superoxide dismutase inhibitor
diethyldithiocarbamic acid abolished the increased
H2O2 and the protection of preconditioning. PKC
activation with phorbol 12-myristate 13-acetate increased cell
survival; the protection of preconditioning was blocked by V1-2, a selective PKC- antagonist.
Similar to preconditioning, the protection of PKC activation was
abolished by mitochondrial KATP channel blockade with
5-hydroxydecanoate or by GABA receptor stimulation with midazolam or
diazepam. In addition, PKC, mitochondrial ATP-sensitive K+
(KATP) channels, and GABA receptors had no effects on
H2O2 generated by ischemic
preconditioning before prolonged hypoxia and reoxygenation. We conclude
that H2O2 opens mitochondrial KATP
channels and inhibits GABA receptors via activating PKC-. Through
this signal transduction, preconditioning protects ischemic cardiomyocytes.
-aminobutyric acid receptors; preconditioning
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