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Interstitial transudate concentration of adenosine and inosine in rat and guinea pig hearts.

Interstitial transudate (IT) was sampled from the surface of isolated constant pressure-perfused guinea pig and rat hearts. With endogenous adenosine (AR) formation, IT concentrations (Crr) of AR and inosine (IR) were 4- to 6.5-fold higher than those in the venous effluent. The AR-to-IR ratio varied between 0.5 and 0.1. During normoxic perfusion, CIT-AR reached a basal level of 0.18 microM. During maintained hypoxia, CIT-AR was elevated only initially up to 0.63 microM. Subsequently, it decreased to basal values, whereas coronary flow remained elevated. With repetitive hypoxia, CIT-AR decreased to basal values, with little alteration in the coronary flow response. Addition of 1,000 U/l adenosine deaminase reduced CIT-AR below 0.2 microM, with no change in coronary flow response to hypoxia. High concentrations of coformycin (Streptomyces antibioticus), an adenosine deaminase inhibitor (greater than 1 microM), were necessary to increase the AR-to-IR ratio to unity, indicating an intracellular site of action. During administration of 0.1 microM dipyridamole, no close correlation between CIT-AR and coronary flow was found. Administration of 1 microM AR did not induce a detectable change in Crr-AR despite a distinct coronary flow response. We conclude that at least in our heart preparation, interstitial adenosine seems to play no primary role in coronary flow regulation.