The temperature dependence of cardioplegic distribution in the canine heart

Background. Cold cardioplegic arrest can produce cooling contracture and su boptimal myocardial protection. This study examines whether cooling contrac ture is associated with maldistribution of cardioplegic solution, particula rly subendocardial hypoperfusion, which may impair recovery. Methods. Canine hearts were arrested by antegrade cold and warm blood cardi oplegia in random order. Cardioplegic distribution was measured using radio labeled microspheres before and just after induction of each period of arre st. Results. With cold cardioplegia, perfusion of left ventricular subepicardia l and midwall regions decreased. Subendocardial to subepicardial perfusion ratios increased significantly in the left ventricle as a whole, the anteri or and posterior regions of the left ventricular free wall, and the interve ntricular septum. With warm arrest, transmural flow distribution was not si gnificantly altered from preceding prearrest values. At constant coronary n ow, coronary perfusion pressure was initially similar after induction of ar rest at both temperatures, but it rose subsequently during warm cardioplegi a. Conclusions. The data suggest that during normothermic arrest, vasomotor to ne regulates cardioplegic distribution, and hyperkalemic vasoconstriction i s of slow onset. In the absence of beating and with vasomotion inhibited by hypothermia, cardioplegic distribution during cold arrest appears to be pr imarily dependent on vascular anatomy. There was no evidence of subendocard ial underperfusion during cooling contracture. (C) 2000 by The Society of T horacic Surgeons.