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Am J Physiol Heart Circ Physiol 254: H1125-H1132, 1988;
0363-6135/88 $5.00
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AJP - Heart and Circulatory Physiology, Vol 254, Issue 6 1125-H1132, Copyright © 1988 by American Physiological Society

ARTICLES

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

U. K. Decking, E. Juengling and H. Kammermeier
Department of Physiology, Medical Faculty of the Technical University, Aachen, Federal Republic of Germany.

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.


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