MYOCARDIAL OXYGENATION DURING TERMINAL WARM BLOOD CARDIOPLEGIA

Background. Terminal warm blood cardioplegia accelerates myocardial me tabolic recovery. The process of myocardial oxygenation during termina l warm blood cardioplegia and its optimal administration are not clear . Methods. We measured the myocardial tissue oxygen saturation (SO2) d uring reperfusion using near-infrared spectroscopy. Twenty-four dogs u nderwent 1 hour of ischaemic arrest with cold crystalloid cardioplegia . They were then divided into four equal groups. Group I dogs received normal blood reperfusion. The other dogs received 15 mL/kg of termina l warm blood cardioplegia at 80 mm Hg in group 2 or at 60 mm Hg in gro up 3, and 30 mL/kg of cardioplegia at 60 mm Hg in group 4, followed by blood reperfusion. Results. In group 1, the SO2 increased gradually d uring the early reperfusion and decreased transiently during the late reperfusion. In group 2, the SO2 increased rapidly but it decreased tr ansiently during blood reperfusion. In groups 3 and 4, the SO2 increas ed rapidly and remained at high levels during the blood reperfusion. R eperfusion ventricular fibrillation occurred along with a SO2 decrease only in groups 1 and 2. The postischemic troponin-T levels of groups 3 and 4 were lower than that of group 1. The functional recovery in gr oup 4 was better than those in the other three groups. Conclusions. Te rminal warm blood cardioplegia accelerates the early SO2 increase and abolishes the SO2 decrease during subsequent reperfusion and reduces t he incidence of reperfusion arrhythmia, suggesting that it ameliorates reperfusion injury and consequently improves postischemic functional recovery. (C) 1998 by The Society of Thoracic Surgeons.