Adenosine antagonist aminophylline attenuates pacing-induced coronary functional hyperemia.

The role of adenosine in pacing-induced hyperemia was examined in 10 dogs. Left coronary blood flow (LCBF), left ventricular O2 extraction [(a-v)O2], and myocardial O2 consumption (MVO2) were monitored. Heart rate (HR) was initially paced at 120 beats/min and then increased to 180 beats/min to elicit a hyperemic response (delta LCBF). During the hyperemia, the vasodilatory response to exogenous adenosine (FAd) was tested. HR was then returned to the initial level, and 20 min after injection of aminophylline (100 mg iv) HR was again increased to 180 beats/min. The response to adenosine was again tested. The pacing-induced increase in MVO2 (delta MVO2) was not affected by aminophylline (P greater than 0.05). However, after aminophylline, the flow response slope delta LCBF/delta MVO2 was decreased by about 20% (P less than 0.05), and the extraction-response slope delta (a-v)O2/delta MVO2 was increased by 100% (P less than 0.05). FAd was also decreased by aminophylline, and the magnitude of the reduction was correlated with the decrease in the flow-response slope (r = 0.82). These results suggest that endogenous adenosine may play an important role in coronary functional hyperemia induced by increases in heart rate.