THE EFFECT OF ANOXIA ON CARDIOMYOCYTE GLUCOSE-TRANSPORT DOES NOT INVOLVE AN ADENOSINE RELEASE OR A CHANGE IN ENERGY-STATE

The action of anoxia on glucose transport was investigated in isolated resting rat cardiomyocytes. Incubation of these cells in the absence of oxygen for 30 min resulted in a 4- to 5-fold increase in glucose tr ansport (with a lag period of 5-10 min). Up to 40 min of anoxia failed to alter the cellular concentrations of ATP, phosphocreatine, and cre atine. Adenosine deaminase (1.5 U/ml), the A(1)-adenosine receptor ant agonist 1,3-diethyl-8-phenylxanthine (1 mu M), or the A(2)-selective a ntagonist 3,7-dimethyl-1-propargylxanthine (20 mu M) had no effect on anoxia-dependent glucose transport. Moreover, adenosine (10-300 mu M, added under normoxia) did not stimulate glucose transport. Wortmannin (1 mu M) did not influence the effect of anoxia, but completely suppre ssed that of insulin On the other hand, the effects of anoxia and insu lin were not additive. These results indicate (i) that the effect of a noxia on cardiomyocyte glucose transport is not mediated by a change i n energy metabolism, nor by an adenosine release; (ii) that it probabl y does not involve a phosphatidylinositol 3-kinase, in contrast to the effect of insulin, and (iii) that the signal chains triggered by anox ia or insulin may converge downstream of this enzyme, or, alternativel y, that anoxic conditions may impair the action of the hormone.