info:eu-repo/semantics/article
Effects of the AMP-activated protein kinase inhibitor compound C on the postconditioned rat heart
Fecha
2012-07Registro en:
Hermann, Romina; Marina Prendes, María Gabriela; Torresin, María Emilia; Vélez, D.; Savino, Enrique Alberto; et al.; Effects of the AMP-activated protein kinase inhibitor compound C on the postconditioned rat heart; Springer Tokyo; Journal Of Physiological Sciences; 62; 4; 7-2012; 333-341
1880-6546
CONICET Digital
CONICET
Autor
Hermann, Romina
Marina Prendes, María Gabriela
Torresin, María Emilia
Vélez, D.
Savino, Enrique Alberto
Varela, Alicia
Resumen
Ischemic postconditioning (IPOC) protects the myocardium from ischemic-reperfusion injury, improving functional recovery and cell viability. This protection is concurrent with stimulation of glycogen breakdown, increased mitochondrial ATP synthesis and content, maintenance of reduced-to-oxidized glutathione ratio (GSH/ GSSG), and decreased oxidative damage. The present study's objective was to assess whether these effects are associated with increased resistance to mitochondrial permeability transition pore (MPTP) opening. The effects of the AMP-activated protein kinase (AMPK) inhibitor, compoundC( CC), were measured to investigate association with AMPK. Mitochondria removed from postconditioned hearts required higher calcium levels to induce MPTP opening. Improved functional recovery, increased glycogen mobilization, maintenance of the GSH/GSSG ratio, decreased oxidative damage, and increased resistance to MPTP opening were abrogated when the hearts were postconditioned in the presence of CC, without affecting preservation of cell viability. Although AMPK appears to play a role in IPOC, it would not be the major cellular mediator. © The Physiological Society of Japan and Springer 2012.