Intracoronary administration of adenosine triphosphate increases myocardial adenosine levels and coronary blood flow in man.

Adenosine triphosphate (ATP) is reported to be released mainly from presynaptic vesicles and cardiomyocytes. The released ATP, which can be degraded to adenosine, may cause coronary vasodilation. However, there is no clear evidence that ATP is degraded to adenosine and causes coronary vasodilation in humans. The present study was undertaken to test whether intracoronary administration of ATP increases myocardial adenosine levels and coronary blood flow. In 11 patients, 3 doses of ATP (0.1, 0.2, and 0.4 mg) were injected into the left anterior descending coronary artery. The velocity of coronary blood flow was measured by Doppler flow probe, and the adenosine concentration in the coronary sinus blood was measured. We also continuously infused ATP (0.2 mg/min) for 1 min in another 10 patients. Coronary blood flow increased dose dependently soon after injection of ATP. Coronary arteriovenous differences in adenosine concentration increased [from 21 +/- 15 to 178 +/- 15 pmol/ml (p < 0.05) 10 sec after the injection of ATP (0.4 mg)] and there were marked reductions in both aortic blood pressure and heart rate. The adenosine levels returned to baseline 20 sec after the injection of ATP, and aortic blood pressure and heart rate also recovered, although coronary blood flow remained increased. Furthermore, continuous infusion of ATP for 1 min increased coronary blood flow velocity and coronary arteriovenous differences in adenosine concentration from 25 +/- 14 to 71 +/- 13 pmol/ml (p < 0.05) in 10 patients. These results indicate that intracoronary administration of ATP immediately increases coronary blood flow and the adenosine concentration of coronary venous blood, which returns to the baseline level thereafter. The differences in the time courses of increases in coronary venous adenosine levels and coronary blood flow after ATP injections suggest that vasodilatory mechanisms other than adenosine, eg, nitric oxide and prostaglandins, may also be involved in the ATP-induced coronary vasodilation. ATP may be used as a cardioprotective agent as well as adenosine.