Coronary Microvascular ß-Adrenoceptor Subtypes and Crystalloid Cardioplegia
To examine the effect of crystalloid cardioplegia on the different β-adrenoceptor subtypes in the coronary microcirculation, we compared microvascular responses before and after cardioplegic arrest. Pigs were placed on cardiopulmonary bypass and hearts were arrested with cold hyperkalemic crystalloid solution. After 1 hour, hearts were reperfused for 1 hour. In vitro coronary arteriolar responses to isoproterenol and the adenylate cyclase activator forskolin were studied in a pressurized, no-flow state with a video-microscopy. After contraction of vessels by 25% to 50% of the baseline diameter, drugs were applied extraluminally. Isoproterenol-induced relaxation of vessels in the presence of ICI-118,551 (ß2-blocker) was significantly less than that of vessels in the presence of atenolol (ß1-blocker). Thus, coronary microvascular relaxation to isoproterenol is primarily due to ß2-adrenoceptor stimulation. Crystalloid cardioplegia reduced relaxations to ß1- or ß2-stimulation and to forskolin. Following reperfusion, the relaxation responses to forskolin and ß1- or ß2-adrenergic stimulation were completely restored. Cardioplegic arrest and reperfusion blunted endothelium-dependent relaxation to adenosine 5′-diphosphate, whereas endothelium-independent relaxation to sodium nitroprusside was not affected. Therefore, the present study demonstrates that crystalloid cardioplegia reduces the ß1- and ß2-adrenoceptor-mediated and cyclic AMP-dependent relaxation in the coronary microcirculation. The cardioplegia-induced alteration in the coronary microvascular ß-adrenergic mechanism may be responsible for episodic coronary spasm and altered myocardial perfusion following cardiac surgery.
KeywordsSodium Nitroprusside Relaxation Response Nitroprusside Sodium Cardioplegic Arrest Coronary Microcirculation
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