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reduces ischemic injury and
does not block protective effects of preconditioning
1 Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, 27709; 2 University of North Carolina, Chapel Hill, 27516; and 3 Duke University Medical Center, Durham, North Carolina 27710
We examined the
effect of inhibition of p38 mitogen-activated protein kinase (MAPK)
/
during ischemia and preconditioning by using the inhibitor
SB-202190. Isolated rat hearts were perfused with Krebs-Henseleit
buffer, while left ventricular developed pressure (LVDP) and
31P nuclear magnetic resonance spectra were acquired
continuously. After 20 min of ischemia and 25 min of reperfusion,
recovery of LVDP in untreated hearts was 32 ± 4%, whereas hearts
treated with SB-202190 5 min before ischemia recovered 59 ± 7%
of their pretreatment LVDP. Preconditioning improved functional
recovery to 65 ± 5%, which was unaffected by SB-202190
treatment, added either throughout the preconditioning protocol
(56 ± 5% recovery) or during the final reperfusion period of
preconditioning (71 ± 11% recovery). Necrosis was assessed after
40 min of ischemia and 2 h of reperfusion using
2,3,5-triphenyltetrazolium chloride (TTC) staining and creatine kinase
release. The untreated group had 54 ± 8% necrotic myocardium, whereas the SB-202190-treated group had 32 ± 7% and the
preconditioned group had 21 ± 4% necrotic tissue by TTC staining.
SB-202190; 31P nuclear magnetic resonance; necrosis; intracellular pH; left ventricular developed pressure
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