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Postconditioning protects reperfused myocardium from ischemia‐damaged mitochondria
Author(s) -
Chen Qun,
Ross Thomas,
Hu Ying,
Lesnefsky Edward
Publication year - 2011
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.25.1_supplement.1097.2
Medical Center, Richmond, VA Mitochondria (MITO) mediate cardiac injury during ischemia (ISC)–reperfusion (REP). The role of mitochondrial damage from ISC to REP injury has remained unclear. We previously showed that most damage to oxidative phosphorylation (OXPHOS) is during ISC. Postconditioning (PC) decreases REP injury by preventing permeability transition pore (MPT) opening. Reversible blockade of electron transport during ISC with amobarbital (AMO) preserves OXPHOS and washes out by 30 sec REP. We asked if PC provides benefit when MITO are protected by AMO during ISC. Langendorff‐perfused Fischer 344 adult (6 mo.) rat hearts underwent 25 min. global ISC and 30 min REP with or without AMO (2.5 mM) for 1 min. immediately before ISC and/or PC (6 cycles of 10 sec ISC‐10 sec REP). MITO were isolated after 30 min REP, and OXPHOS and calcium retention capacity (CRC) measured. AMO and AMO+PC preserved OXPHOS (glutamate as a complex I substrate) vs. untreated ISC‐REP hearts, whereas PC alone did not. AMO, PC, and AMO+PC decreased LDH release during REP although LDH release in PC alone was greater than AMO and AMO+PC. AMO, PC, and AMO+PC improved CRC. Again, CRC protection by PC was less than AMO and AMO+PC (table). Thus, when MITO are protected during ISC, additional intervention at the onset of REP is not needed to decrease injury. PC likely protects during REP by modulating MITO damaged by preceding ISC.