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Stunned myocardium" is defined as the prolonged but transient postischemic contractile dysfunction of viable myocardium that has been salvaged by reperfusion. This phenomenon, although first characterized in the experimental canine model of coronary artery occlusion/reperfusion, also occurs following transient global
ischemia. Moreover, despite the superb cardioprotection conferred by administration of cold
cardioplegia during aortic cross-clamping,
stunned myocardium is a well-recognized sequela of prolonged
cardiopulmonary bypass. Using the anesthetized 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 development of
stunned myocardium following bypass. Thirteen dogs were placed 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-hour cross-clamp period. Left ventricular (LV) systolic function (i.e., area LV ejection fraction and posterior LV free wall thickening assessed by two-dimensional echocardiography) 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 electron microscopic analysis. All dogs in both treatment groups showed electron microscopic evidence of mild and reversible morphological injury indicative of
stunned myocardium, with no difference between dogs that received warm versus cold
cardioplegia. Direct comparison of LV function between the two groups was confounded by a profound decrease in afterload in dogs that received cold
cardioplegia. However, incorporation of systemic vascular resistance as a covariate revealed that LV function following bypass was modestly depressed at approximately 85% of baseline values, and that continuous administration of warm
cardioplegia did not prevent this hypokinesis. Thus, in our canine model: (1) morphological injury and
LV dysfunction induced by 3 hours of aortic cross-clamping is subtle; and (2) continuous retrograde infusion of warm blood
cardioplegia during the cross-clamp period failed to preclude
myocardial stunning following prolonged
cardiopulmonary bypass.