Effects of dipyridamole on myocardial adenosine and active hyperemia

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Abstract
Dipyridamole, a vasodilator that potentiates the actions of exogenous adenosine, is known to inhibit cellular uptake of adenosine, but its effects on cellular adenosine release, and interstitial adenosine levels, are disputed. The accumulation of adenosine in pericardial infusates (PCI) was used as an index of interstitial adenosine concentration and the effects of dipyridamole on relationships among [canine] coronary blood flow (CBF), myocardial O2 consumption (M.ovrhdot.VO2), and PCI adenosine concentrations were observed during steady-state alterations of cardiac work. Dipyridamole increased CBF and PCI adenosine concentration without altering M.ovrhdot.VO2. The relationship between PCI adenosine and CBF was unaltered, supporting a cause and effect relationship beteeen interstitial adenosine concentration and CBF. Unlike previous studies in isolated perfused hearts the washout of adenosine by coronary plasma was unaffected by dipyridamole. Whereas dipyridamole inhibits adenosine uptake, it apparently does not alter cellular adenosine release, and interstitial adenosine levels are increased. The constant relationship between PCI adenosine and CBF supports hypotheses that attribute the hyperemias associated with increased cardiac work or with dipyridamole to increased interstitial adenosine.