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- W164751722 abstract "Myocardial ischemia (ISC) damages the electron transport chain (ETC). Blockade of the ETC during ISC at complex I with amobarbital (AMO) protects against ETC damage during ISC and decreases necrosis measured after reperfusion (REP). Opening of the mitochondrial permeability transition pore (MPTP) is a key mechanism of REP injury. We hypothesized that ischemic ETC damage leads to MPTP opening as a mechanism of REP injury. Isolated rabbit hearts were perfused for 15 min. followed by 30 min. stop-flow ISC at 37°C (ISC alone) or given 2.5 mM AMO for 1 min. immediately before ISC. Subsarcolemmal mitochondria (SSM) were isolated after ISC. AMO treatment protected respiration (nAO/mg/min) with glutamate (complex I) and TMPD-ascorbate (complex IV) as substrates. MPTP opening was assessed by detecting mitochondrial swelling by 200 uM calcium (% change of AU/mg/min). AMO inhibition of ETC during ISC attenuated swelling of SSM. Protection of the ETC during ISC significantly decreased MPTP opening. Ischemic damage to ETC promotes MPTP opening as a mechanism of mitochondrial-dependent cardiac injury during REP, translating ischemic ETC damage into REP injury. SSM Glutamate TMPD-asc Swelling ISC (n=5) 110±9 360±21 15.1±3.4 AMO (n=4) 185±29* 554±17* 4.0±1.8* ±SEM; *p<0.05 vs. ISC" @default.
- W164751722 created "2016-06-24" @default.
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- W164751722 date "2008-03-01" @default.
- W164751722 modified "2023-10-14" @default.
- W164751722 title "Ischemic damage to the mitochondrial electron transport chain favors opening of the permeability transition pore" @default.
- W164751722 doi "https://doi.org/10.1096/fasebj.22.1_supplement.750.6" @default.
- W164751722 hasPublicationYear "2008" @default.
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