الفهرس 
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Abstract
The underlying reasons for the impaired cardiac function after cardioplegic arrest and cardiopulmonary bypass can be explained on the basis of the pathophysiology related to the cardiopulmonary bypass. Protection of the myocardium against ischemia during cardiac surgery, such as that induced with aortic cross-clamping, is accomplished with the use of hyperkalemic and/or hypothermic cardiac arrest. However, recent investigations on the cellular pathophysiology of ischemic injury have consistently demonstrated that a significant portion of the damage occurs not only during the period of myocardial ischemia, but during the reperfusion period in an attempt to salvage the myocardium. This injury has been termed “ischemic reperfusion injury”, and is probably responsible for the prolonged cardiac dysfunction or “myocardial stunning” after the termination of the cardiopulmonary bypass.
Single or multiple brief periods of preceding ischemia that produce sublethal myocyte injury have been shown to decrease the infarct size, limit the degree of myocardial dysfunction, and reduce the incidence of cardiac arrhythmias after a subsequent and more prolonged period of myocardial ischemia (i.e. aortic cross-clamp). This phenomenon has been termed ischemic preconditioning to protect against ischemic reperfusion injury.
Sevoflurane, the inhalational anesthetic, has been shown to induce the same effect as ischemic preconditioning based on many animal studies. Sevoflurane administration prior to the ischemic period appears to mimic the cardioprotective effects of ischemic preconditioning.
Forty adult patients scheduled for CABG for multiple vessel disease were randomly assigned to two equal groups each of 20 patients; the Sevoflurane group and control group. Patients of the sevoflurane