A sustained rise in intracellular calcium during ischemia and lack of recovery during reperfusion is associated with irreversible cell injury and death.
Understanding the mechanisms responsible for the rise in Ca(2+) during ischemia and early reperfusion could have important therapeutic implications for reducing cell death.
During ischemia, ATP and phosphocreatine (PCr) decline, whereas intracellular hydrogen ion, intracellular sodium (Na(+)), calcium (Ca(2+)), and magnesium (Mg(2+)) concentrations all rise. If the ischemia is relatively short and there is little irreversible injury (cell death), PCr, pH, Na(+), Mg(2+), and Ca(2+) all recovery quickly on reperfusion. ATP recovery can take up to 24 h because of loss of adenine base from the cell and the need for de novo synthesis. There are correlative data showing that a sustained rise in Ca(2+) during ischemia and/or lack of recovery during reperfusion is associated with irreversible cell injury. Interventions that reduce the rise in Ca(2+) during ischemia and reperfusion have been shown to reduce cell death. Therefore, a better understanding of the mechanisms responsible for the rise in Ca(2+) during ischemia and early reperfusion could have important therapeutic implications. This review will discuss mechanisms involved in alterations in ions and high energy phosphate metabolites in perfused or intact heart during ischemia and reperfusion.
Murphy et al. (Tue,) conducted a review in Ischemia and reperfusion injury. A sustained rise in intracellular calcium during ischemia and lack of recovery during reperfusion is associated with irreversible cell injury and death.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: