ADRENERGIC REGULATION OF CORONARY MICROCIRCULATION AFTER EXTRACORPOREAL-CIRCULATION AND CRYSTALLOID CARDIOPLEGIA

The purpose of the present study was to examine whether adrenoceptor-m ediated responses of porcine coronary resistance arteries are affected by cardioplegic arrest under conditions of extracorporeal circulation (cardiopulmonary bypass; CPB). Pigs were placed on CPB. The hearts we re arrested with a cold hyperkalemic crystalloid cardioplegic solution for 1 h, then were reperfused for 1 h. In vivo and in vitro beta-adre noceptor-mediated responses were compared before CPB and 2 min and 1 h after initiation of reperfusion. In vitro responses were studied in a pressurized no-flow state with video microscopy. Isoproterenol (0.02 mu g.kg(-1)min(-1), intracoronary) increased coronary blood flow by 10 0 +/- 32% (P < 0.001) before CPB and cardioplegic arrest, 17 +/- 7% 2 min postcardioplegia (P < 0.01), and 71 +/- 9 (P < 0.001) after 1 h of reperfusion. Relaxation of precontracted microvessels (90-180 mu m) t o isoproterenol, NaF, forskolin, and adenosine was reduced after cardi oplegic arrest (all P < 0.001). After 1 h of postcardioplegia-reperfus ion, relaxation responses to forskolin and adenosine were completely r estored, whereas the responses to isoproterenol (P < 0.05) and NaF (P < 0.10) were only partially recovered. Cardioplegic arrest and postcar dioplegia-reperfusion blunted the alpha(2)-adrenoceptor-mediated endot helium-dependent relaxation to clonidine (P < 0.001) but did not affec t the minimal (< 4%) contractile response to the alpha(1)-adrenoceptor agonist phenylephrine or the relaxation to nitroprusside. These resul ts show that hyperkalemic cardioplegia results in the generalized defe ct in the beta-adrenoceptor-G(s) protein-adenylate cyclase pathway, wh ich is significantly restored after reperfusion.