STUNNED MYOCARDIUM FOLLOWING PROLONGED CARDIOPULMONARY BYPASS - EFFECT OF WARM VERSUS COLD CARDIOPLEGIA IN THE CANINE MODEL

''Stunned myocardium'' is defined as the prolonged but transient posti schemic contractile dysfunction of viable myocardium that has been sal vaged by reperfusion. This phenomenon, although first characterized in the experimental canine model of coronary artery occlusion/reperfusio n, also occurs following transient global ischemia. Moreover, despite the superb cardioprotection conferred by administration of cold cardio plegia during aortic cross-clamping, stunned myocardium is a well-reco gnized sequela of prolonged cardiopulmonary bypass. Using the anesthet ized open chest dog, we tested the concept that continuous retrograde infusion of warm blood cardioplegia would effectively prevent ischemia during prolonged aortic cross-clamping and thereby preclude the devel opment of stunned myocardium following bypass. Thirteen dogs were plac ed on cardiopulmonary bypass and randomized to receive: (1) continuous retrograde administration of warm blood cardioplegia (n = 8); or (2) intermittent retrograde cold blood cardioplegia (n = 5) during a 3-hou r cross-clamp period. Left ventricular (LV) systolic function (i.e., a rea LV ejection fraction and posterior LV free wall thickening assesse d by two-dimensional echocardlography) and hemodynamic parameters were monitored at baseline and at 1 and 2 hours postbypass and, at the end of the protocol, transmural myocardial biopsies were obtained for ele ctron microscopic analysis. All dogs in both treatment groups showed e lectron microscopic evidence of mild and reversible morphological inju ry indicative of stunned myocardium, with no difference between dogs t hat received warm versus cold cardioplegia. Direct comparison of LV fu nction between the two groups was confounded by a profound decrease in afterload in dogs that received cold cardioplegia. However, incorpora tion of systemic vascular resistance as a covariate revealed that LV f unction following bypass was modestly depressed at approximately 85% o f baseline values, and that continuous administration of warm cardiopl egia did not prevent this hypokinesis. Thus, in our canine model: (1) morphological injury and LV dysfunction induced by 3 hours of aortic c ross-clamping is subtle; and (2) continuous retrograde infusion of war m blood cardioplegia during the cross-clamp period failed to preclude myocardial stunning following prolonged cardiopulmonary bypass.