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 transport (with a lag period of 5-10 min). Up to 40 min of anoxia failed to alter the cellular concentrations of ATP, phosphocreatine, and creatine. Adenosine deaminase (1.5 U/ml), the A₁-adenosine receptor antagonist 1,3-diethyl-8- phenylxenthine (1 μM), or the A₂-selective antagonist 3,7-dimethyl-1- propargylxanthine (20 μM) had no effect on anoxia-dependent glucose transport. Moreover, adenosine (10-300 μM, added under normoxia) did not stimulate glucose transport. Wortmannin (1 μM) did not influence the effect of anoxia, but completely suppressed that of insulin. On the other hand, the effects of anoxia and insulin were not additive. These results indicate (i) that the effect of enoxia on cardiomyocyte glucose transport is not mediated by a change in energy metabolism, nor by an adenosine release; (ii) that it probably does not involve a phoshatidylinositol 3-kinase, in contrast to the effect of insulin, and (iii) that the signal chains triggered by anoxia or insulin may converge downstream of this enzyme, or, alternatively, that anoxic conditions may impair the action of the hormone.