Abstract

Preservation of myocardial high-energy phosphates correlates with the heart's ability to resume normal function following aortic crossclamping (AXC). The ability of the canine myocardium to synthesize and maintain ATP during 180 minutes of AXC was evaluated in 12 hearts subjected to either blood or crystalloid cardioplegic arrest. Group 1 hearts were arrested by infusion of 750 ml of blood potassium cardioplegia (BKC) solution into the aortic root initially and every 30 minutes, as were group 2 (six) hearts but with a crystalloid cardioplegia (CC) solution. Transmural left ventricular biopsy specimens were obtained for ATP analysis prior to AXC (control), before and after cardioplegia injections 2, 4, and 6, prior to unclamping (180 minutes of AXC), and 30 minutes following reperfusion. ATP levels increased significantly above control (p less than 0.005) during the 180 minutes of AXC immediately following infusion of BKC. At the end of 180 minutes of AXC and following 30 minutes of reperfusion, ATP was noted to be normal in this group (p = NS). In contrast, ATP levels fell significantly (p less than 0.005) during the period of aortic cross-clamping in the crystalloid cardioplegia group and did not return to normal even after 30 minutes of reperfusion (p less than 0.005). We concluded that BKC, by presenting the arrested myocyte with adequate oxygen and substrate, allows for synthesis and preservation of myocardial ATP during periods of AXC as long as three hours. In this respect, it should be regarded as superior to CC, which permits a statistically significant depletion of ATP (p less than 0.005) uncorrected, even after 30 minutes of reperfusion in the beating, nonworking state.

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