Role of adenosine in postischemic dysfunction of coronary innervation.

We sought to determine the role of adenosine in the sustained but reversible decrease in cardiac neurotransmission that occurs after brief ischemia. Adult mongrel dogs were anesthetized and instrumented for measurements of heart rate, arterial pressure, and left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX) flow velocities. Changes in coronary vascular resistance were measured during bilateral stimulation of the stellate ganglia. After beta-adrenergic blockade and bilateral vagotomy, stellate stimulation increased coronary vascular resistance in the LAD and LCX beds 28 +/- 2% and 30 +/- 3%, respectively. After a 15-minute infusion of adenosine into the LAD, the peak increase in LAD resistance was significantly reduced (18 +/- 2%) compared with LCX (34 +/- 5%) and control (P < .05, n = 6) resistance. The LAD response after infusion of the vasodilator papaverine was unchanged (n = 6). Intracoronary infusion of adenosine deaminase (n = 10) but not vehicle (n = 5) into the LAD during a 15-minute LAD occlusion prevented the attenuation in constriction to stellate stimulation. We conclude that adenosine, exogenously infused or endogenously produced, is capable of reducing cardiac neurotransmission.