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Postconditioning during reperfusion attenuates myocardial injury without improved mitochondrial oxidative phosphorylation
Author(s) -
Chen Qun,
Lesnefsky Edward J
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.763.5
Subject(s) - oxidative phosphorylation , mitochondrion , cytochrome c oxidase , chemistry , ischemia , reperfusion injury , phosphorylation , succinate dehydrogenase , respiration , medicine , biochemistry , anatomy
Postconditioning (PC) applied during reperfusion (REP) decreases myocardial injury. However, mitochondrial damage occurs during ischemia (ISC). We propose that PC can not improve ISC‐damaged mitochondrial function during REP. In the untreated group (UNT), isolated rat hearts were subjected to 30 min global ISC and 30 min REP at 37°C. In the PC group, 6 cycles of 10 sec ISC + 10 sec REP was applied at the onset of REP. Subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM) were isolated at the end of REP. Maximal state 3 rates of oxidative phosphorylation (OXPHOS, nAO/mg/min) were measured. PC decreased LDH release (mu/g/60 min; UNT 1065±182 vs. PC 669±38 n=5 in each group P < 0.05) without improved functional recovery during REP. PC did not improve respiration in SSM and IFM using glutamate, succinate, and TMPD‐ascorbate as complex I, complex II, and cytochrome oxidase substrates, respectively. Thus, cardiac injury can still be attenuated even though OXPHOS are already compromised by ISC. The mechanism by which PC decreases myocardial injury is not through improved OXPHOS. ±SEM; *p<0.05 vs. UNT (untreated), TC, time control