Ischemic preconditioning does not protect via blockade of electron transport.
J Appl Physiol (1985)
; 103(2): 623-8, 2007 Aug.
Article
em En
| MEDLINE
| ID: mdl-17463293
ABSTRACT
Ischemic preconditioning (IPC) before sustained ischemia decreases myocardial infarct size mediated in part via protection of cardiac mitochondria. Reversible blockade of electron transport at complex I immediately before sustained ischemia also preserves mitochondrial respiration and decreases infarct size. We proposed that IPC would attenuate electron transport from complex I as a potential effector mechanism of cardioprotection. Isolated, Langendorff-perfused rat hearts underwent IPC (3 cycles of 5-min 37 degrees C global ischemia and 5-min reperfusion) or were perfused for 40 min without ischemia as controls. Subsarcolemmal (SSM) and interfibrillar (IFM) populations of mitochondria were isolated. IPC did not decrease ADP-stimulated respiration measured in intact mitochondria using substrates that donate reducing equivalents to complex I. Maximally expressed complex I activity measured as rotenone-sensitive NADHubiquinone oxidoreductase in detergent-solubilized mitochondria was also unaffected by IPC. Thus the protection of IPC does not occur as a consequence of a partial decrease in complex I activity leading to a decrease in integrated respiration through complex I. IPC and blockade of electron transport both converge on mitochondria as effectors of cardioprotection; however, each modulates mitochondrial metabolism during ischemia by different mechanisms to achieve cardioprotection.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Precondicionamento Isquêmico Miocárdico
/
Complexo I de Transporte de Elétrons
/
Mitocôndrias Cardíacas
Limite:
Animals
Idioma:
En
Revista:
J Appl Physiol (1985)
Assunto da revista:
FISIOLOGIA
Ano de publicação:
2007
Tipo de documento:
Article
País de afiliação:
Estados Unidos