Reoxygenation of guinea pig ventricular myocytes caused mitochondrial depolarization and elevated intramitochondrial Ca2+, which correlated with the likelihood of hypercontracture.
Ca2+-dependent mitochondrial depolarization during reoxygenation may play a significant role in promoting irreversible cell injury in cardiac muscle.
The aim of this study was to investigate the role of mitochondrial ionic homeostasis in promoting reoxygenation-induced hypercontracture in cardiac muscle. Mitochondrial membrane potential and intramitochondrial Ca2+ concentration (Ca2+) were measured using confocal imaging in guinea pig ventricular myocytes exposed to anoxia and reoxygenation. Anoxia produced a variable, but often profound, mitochondrial depolarization. Some cells mounted a recovery of their mitochondrial membrane potential during reoxygenation; the depolarization was sustained in other cells. Recovery of the mitochondrial membrane potential seemed essential to avoid reoxygenation-induced hypercontracture. Reoxygenation also caused a sizable elevation in intramitochondrial Ca2+, the amplitude of which was correlated with the likelihood of a cell undergoing hypercontracture. A sustained Ca2+ load analogous to that seen during reoxygenation was imposed on cardiac mitochondria through permeabilization of the plasma membrane. Elevation of intracellular Ca2+ to 800 nM caused a substantial mitochondrial depolarization. We propose that the conditions seen in guinea pig ventricular myocytes during reoxygenation are well suited to produce Ca2+-dependent mitochondrial depolarization, which may play a significant role in promoting irreversible cell injury.
Delcamp et al. (Sat,) conducted a other in Anoxia-reoxygenation injury. Anoxia and reoxygenation was evaluated on Mitochondrial membrane potential and intramitochondrial Ca2+ concentration. Reoxygenation of guinea pig ventricular myocytes caused mitochondrial depolarization and elevated intramitochondrial Ca2+, which correlated with the likelihood of hypercontracture.