Abstract
A high concentration (12mM) of magnesium (Mg) during hypoxia accelerated reoxygenation-induced contractile recovery and improved the final level of pressure development in an isolated rat heart. This protective effect of Mg was not solely due to its effect as a “natural Ca blocker”, but seemed due to the opening of the mitochondrial KATP channel. High Mg-treated myocytes showed morphologically intact mitochondria and ther membrane potential remained near normal after prolonged hypoxia-reoxygenation.
