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Myocardial protection by volatile anesthetics in patients undergoing cardiac surgery: a critical review of the laboratory and clinical evidence.

JOHN BLAND AND EDWARD LOWENSTEIN first reported in 1976 that administration of halothane (0.75 minimum alveolar concentration [MAC]) significantly (p o 0.001) attenuates ST-segment elevation caused by brief coronary artery occlusion in 6 dogs anesthetized with chloraloseurethane concomitant with a reduction in the primary determinants of myocardial oxygen consumption. These experiments demonstrated, for the first time, that volatile anesthetics are capable of producing essential anti-ischemic effects. Since the publication of this landmark paper, several studies provided further evidence that volatile anesthetics protected myocardium against reversible and irreversible ischemic injury. For example, isoflurane and halothane enhanced the functional recovery of postischemic-reperfused (‘‘stunned’’) canine myocardium when either volatile anesthetic was administered before a 15-min coronary artery occlusion and reperfusion. This beneficial effect occurred in conjunction with the preservation of high-energy phosphates. Isoflurane also reduced the magnitude of myocardial necrosis and improved recovery of left ventricular (LV) function after global ischemia and reperfusion. Halothane was shown to maintain contractile function and ultrastructural integrity during reperfusion after normothermic cardioplegic arrest in isolated rat hearts. These results were especially notable because they implied that the protective action of volatile anesthetics occur independent of any favorable alteration in coronary perfusion or myocardial oxygen supply-demand relations. In 1997, three research groups simultaneously reported that the administration of halothane or isoflurane before prolonged coronary artery occlusion and reperfusion reduced myocardial infarct size in vivo. This beneficial effect was termed ‘‘anesthetic preconditioning’’ (APC), occurred independent of changes in systemic and coronary hemodynamics, and persisted despite discontinuation of the volatile anesthetic before coronary artery occlusion, a ‘‘memory’’ period similar to that observed during ischemic preconditioning (IPC). Subsequently, volatile anesthetics were shown to protect myocardium against ischemic