A COMPARISON OF AMP DEGRADATION IN THE PERFUSED RAT-HEART DURING 2-DEOXY-D-GLUCOSE PERFUSION AND ANOXIA .1. THE RELEASE OF ADENOSINE AND INOSINE

AMP degradation is studied in two models of the Langendorff-perfused r at heart which generate a large release of purines: the 2-deoxy-D-gluc ose (2DG)-perfused heart and the anoxic heart. In the 2DG model, mitoc hondrial energy generation is quasi-normal, despite a very low ATP con centration. Furthermore, inorganic phosphate (P-i) concentration is lo w, an important difference with anoxia where P-i is very high, up to 8 2 mM. Coronary release of purines is measured by high performance liqu id chromatography, and myocardial metabolite content by P-31 nuclear m agnetic resonance spectroscopy. In the 2DG-perfused hearts with glucos e or acetate, the purine release consists nearly exclusively of inosin e [up to 130 nmol/(min x gww)] while adenosine is less than 1 nmol/(mi n x gww). A possible interpretation is that AMP degradation proceeds m ainly through deamination to inosine monophosphate by AMP deaminase (t he IMP pathway). In contrast, the purine release in anoxia (100% N-2) contains comparable quantities of adenosine and inosine [respectively 30 and 20 nmol/(min x gww)], indicating that part of AMP is dephosphor ylated directly to adenosine. Comparison with the 2DG model suggests t hat the release of adenosine in the anoxic heart is a result of inhibi tion of AMP deaminase by P-i. (C) 1996 Academic Press Limited