THE ELECTROPHYSIOLOGY OF ISCHEMIA AND CARDIOPLEGIA - IMPLICATIONS FORMYOCARDIAL PROTECTION

The primary goal of modern cardioplegia is to protect the heart during the periods of cardiac arrest and global ischemia that are required t o perform cardiac surgery, In order to achieve this, cardioplegic solu tions must be able to arrest rapidly the electrical activity of the he art, An understanding of the electrophysiology of cardioplegia is crit ical to an adequate understanding of its basic mechanisms of action. T his article reviews recent advances in our understanding of the electr ophysiological changes seen during ischemia and cardioplegia. Although 10 years ago, depolarization and repolarization were attributed to ch anges in membrane resistance, advances in molecular biology have eluci dated that the mechanism of the action potential is governed by ionic transport across hydrophobic lipid membranes through carefully regulat ed pores formed by members of an extended family of ion channel protei ns, There also have been great strides in our understanding of the hea rt's electrophysiological response to ischemia, One of the most dramat ic responses to ischemia is a profound shortening of the cardiac actio n potential, which has been shown to be cardioprotective by limiting c alcium influx into the cell, ATP-sensitive potassium channels have bee n confirmed to play a critical role in the action potential shortening seen during ischemia, Drugs that open these channels have been shown to limit infarct size, attenuate myocardial stunning, and ameliorate r eperfusion injury. Recent work has demonstrated that these drugs may b e effective cardioplegic agents. This approach is just one example of a cardioplegic strategy that exploits the new knowledge provided by re cent advances in our understanding of cellular ion transport systems.