Blood and albumin cardioplegia preserve endothelium-dependent microvascular responses

Alterations of vascular reactivity may be a cause of reduced myocardial perfusion after cardioplegic arrest. The effects of blood and albumin cardioplegia on endothelium-dependent coronary microvascular function and ultrastructure were examined after cardiopulmonary bypass, ischemic arrest, and reperfusion. During cardiopulmonary bypass, porcine hearts were arrested with either blood, albumin-crystalloid, or crystalloid cardioplegia for 1 hour, followed with reperfusion for 1 hour. Noninstrumented pigs were used as controls. Coronary microarterial vessels (90 to 190 microns in diameter) were studied in a pressurized, no-flow state with video microscopic imaging and electronic dimension analysis. Ischemic arrest with crystalloid cardioplegia markedly reduced endothelium-dependent relaxations to the adenine nucleotide adenosine diphosphate and the calcium ionophore A23187. Enhanced contractile responses were observed to the platelet-derived vasoactive substance serotonin and to the thromboxane A2 analogue U46619. Indomethacin corrected the enhanced contractile responses to serotonin, indicating the enhanced release of a constrictor prostanoid substance. Indomethacin had no effect on the impaired relaxations to adenosine diphosphate or A23187. Endothelium-dependent relaxations to adenosine diphosphate, serotonin, and A23187 were significantly preserved with either blood or albumin-crystalloid cardioplegia, whereas contractile responses to U46619 were normal. Endothelium-independent relaxation to nitroprusside was similar in all groups, indicating normal smooth muscle responsiveness. Electron microscopy revealed minimal alterations of vascular morphology of vessels in both crystalloid and blood cardioplegia groups.(ABSTRACT TRUNCATED AT 250 WORDS)