Myocardial oxygenation during terminal warm blood cardioplegia.

Abstract

Terminal warm blood cardioplegia accelerates myocardial metabolic recovery. The process of myocardial oxygenation during terminal warm blood cardioplegia and its optimal administration are not clear. We measured the myocardial tissue oxygen saturation (SO2) during reperfusion using near-infrared spectroscopy. Twenty-four dogs underwent 1 hour of ischemic arrest with cold crystalloid cardioplegia. They were then divided into four equal groups. Group 1 dogs received normal blood reperfusion. The other dogs received 15 mL/kg of terminal warm blood cardioplegia at 80 mm Hg in group 2 or at 60 mm Hg in group 3, and 30 mL/kg of cardioplegia at 60 mm Hg in group 4, followed by blood reperfusion. In group 1, the SO2 increased gradually during the early reperfusion and decreased transiently during the late reperfusion. In group 2, the SO2 increased rapidly but it decreased transiently during blood reperfusion. In groups 3 and 4, the SO2 increased rapidly and remained at high levels during the blood reperfusion. Reperfusion 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 group 4 was better than those in the other three groups. Terminal warm blood cardioplegia accelerates the early SO2 increase and abolishes the SO2 decrease during subsequent reperfusion and reduces the incidence of reperfusion arrhythmia, suggesting that it ameliorates reperfusion injury and consequently improves postischemic functional recovery.