Effect of aminophylline on coronary functional hyperemia and myocardial adenosine

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Abstract
The role of adenosine in coronary functional hyperemia was tested using the adenosine antagonist aminophylline. In 11 dogs left coronary blood flow (LCBF) and left ventricular O2 extraction [(a-v)O2] were monitored. Myocardial O2 consumption (M.ovrhdot.VO2) was calculated. Before aminophylline was administered, intracoronary infusion of 6.8 .mu.g/min norepinephrine increased LCBF and M.ovrhdot.VO2 by 40-80%. Simultaneous infusion of adenosine further increased LCBF. Fifteen min after injection of 100 mg aminophylline, norepinephrine still increased LCBF, and the ratio .DELTA.LCBF/.DELTA.M.ovrhdot.VO2 was unchanged (P > 0.05). Although the functional hyperemia was not blunted, the response to infused adenosine was abolished by aminophylline. In 20 additional dogs myocardial adenosine was determined. Before norepinephrine infusion myocardial adenosine with and without aminophylline was 12.7 and 14.3 nmol/g dry wt, respectively (P > 0.05). During norepinephrine infusion an increase in adenosine correlated well with increases in M.ovrhdot.VO2 and LCBF, but the increase in adenosine was not greater after aminophylline. The failure of aminophylline to blunt functional hyperemia was not due to a higher adenosine level after aminophylline. A role for adenosine in functional hyperemia elicited by norepinephrine is not supported.

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