The primary goal of modern cardioplegia is to protect the heart during the periods of cardiac arrest and global ischemia that are required to perform cardiac surgery. In order to achieve this, cardioplegic solutions must be able to arrest rapidly the electrical activity of the heart. An understanding of the electrophysiology of cardioplegia is critical to an adequate understanding of its basic mechanisms of action. This article reviews recent advances in our understanding of the electrophysiological changes seen during ischemia and cardioplegia. Although 10 years ago, depolarization and repolarization were attributed to changes in membrane resistance, advances in molecular biology have elucidated that the mechanism of the action potential is governed by ionic transport across hydrophobic lipid membranes through carefully regulated pores formed by members of an extended family of ion channel proteins. There also have been great strides in our understanding of the heart's electrophysiological response to ischemia. One of the most dramatic responses to ischemia is a profound shortening of the cardiac action potential, which has been shown to be cardioprotective by limiting calcium influx into the cell. ATP‐sensitive potassium channels have been 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 reperfusion injury. Recent work has demonstrated that these drugs may be effective cardioplegic agents. This approach is just one example of a cardioplegic strategy that exploits the new knowledge provided by recent advances in our understanding of cellular ion transport systems.
|Number of pages||9|
|Journal||Journal of cardiac surgery|
|State||Published - Jul 1995|