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Myogenic reactivity of coronary resistance arteries after cardiopulmonary bypass and hyperkalemic cardioplegia

, : Myogenic reactivity of coronary resistance arteries after cardiopulmonary bypass and hyperkalemic cardioplegia. Circulation 92(6): 1590-1596

Background: Cardiopulmonary bypass (CPB) and cardioplegia are associated with systemic hypotension and altered vascular responses, suggesting a defect in the smooth muscle control of vascular tone. Previous studies demonstrated alteration in neurohumoral control of the systemic and coronary circulation after CPB and cardioplegia; however, effects of CPB and cardioplegia on the intrinsic control of the vascular smooth muscle, especially in the coronary microcirculation, remain to be determined. Methods and Results: Pigs were placed on CPB. Selected hearts were arrested with a cold, hyperkalemic ((K+)=25 mmol/L) crystalloid cardioplegic solution for 1 hour. In another group, hearts were arrested and then reperfused with warm blood for 1 hour. Coronary arterioles (70 to 149 mu-m) were studied in a pressurized, no-flow state with video microscopy. Myogenic reactivity was examined to stepwise increases in intraluminal pressure from 10 to 100 mm Hg. The vessel diameter was normalized to the diameter at 50 mm Hg after application of papaverine (10-4 mol/L). Myogenic reactivity of vessels from noninstrumented control pigs was not altered after mechanical denudation of the endothelium or pretreatment with N-G-nitro-L-arginine or indomethacin. In vessels from control pigs and vessels from the CPB group, myogenic contraction was observed with pressures gt 40 mm Hg. However, CPB significantly decreased intrinsic tone as the pressure-diameter relation shifted upward (P lt .05 versus control). This decreased intrinsic tone was markedly attenuated by N-G-nitro-L-arginine, suggesting an increased basal release of nitric oxide. Cardioplegic arrest, with or without reperfusion, decreased myogenic contraction to pressures gt 40 mm Hg (P lt .05 versus control). Pretreatment of vessels with glibenclamide normalized the cardioplegia-induced decrease in myogenic contraction (P lt .05), suggesting that the reduced myogenic contraction is due to activation of ATP-sensitive potassium channels. Conclusions: The result of the present study suggests that coronary microvascular myogenic reactivity and the intrinsic tone are reduced after hyperkalemic cardioplegia and that CPB preserves myogenic reactivity but reduces the intrinsic tone of the vascular smooth muscle.


PMID: 7664445

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