Title: Postconditioning reduces infarct size and oxidative stress via mitochondrial KATP channel activation
Abstract: This study tested the hypothesis that inhibition of myocardial injury and oxidative stress with postconditioning (PostC) is related to activation of mitochondrial (mito-)KATP channels. 30 canines undergoing 60 min of ischemia and 24 h of reperfusion (R) were randomly divided into: Control (n=10): no intervention at R; PostC (n=8): 3 cycles of 30 s R alternating with 30 s re-occlusion were applied at the onset of R; 5-hydroxydecanoate (5-HD, n=6): the mito-KATP channel blocker, 5-HD was infused before PostC; HMR1098 (n=6): the sarcolemmal KATP channel blocker, HMR1098 was infused before PostC. Infarct size was smaller in PostC relative to Control group (27±4% vs. 39±2%). The infarct-sparing effect of PostC was blocked by 5-HD (48±5%†), but was not by HMR1098 (29±3%). Superoxide anion detected by chemiluminescence (CL) from coronary venous blood was reduced in both PostC and HMR1098 groups compared to Control and 5-HD groups. A 52±5% reduction in CL from blood after depleting neutrophils (PMNs) suggested that the PMNs are the main source of superoxide anion. In H9c2 cells of 8 h hypoxia and 3 h of reoxygenation, PostC maintained mitochondrial membrane potential and inhibited permeability transition pore (mPTP) opening evidenced by preserved TMRE and calcein fluorescent staining, which was blocked by 5-HD, but not by HMR1098. These data suggest that PostC reduces infarct size and decreases superoxide anion largely by opening mito-KATP channel and inhibiting mPTP opening. p<0.05 vs. Control; +p<0.05 vs. PostC.
Publication Year: 2007
Publication Date: 2007-06-01
Language: en
Type: article
Indexed In: ['crossref']
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Cited By Count: 2
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