Myocardial glucose uptake and breakdown during adenosine-induced vasodilation

Abstract

In isolated K⁺ (16.2 mM)-arrested cat hearts perfused at constant pressure adenosine infusions (0.8 μmoles · min⁻¹ · 100 g⁻¹ for 10 min) caused an increase in myocardial¹⁴C-glucose uptake and release of¹⁴CO₂+H¹⁴CO ₋ ³ and¹⁴C-lactate simultaneously with a rise in coronary flow. The ratio of the release of¹⁴CO₂+H¹⁴CO ₋ ³ to that of¹⁴C-lactate and the specific activity of lactate in the effluate were not altered. In K⁺-arrested hearts perfused with constant volume neither glucose uptake nor glucose breakdown were influenced by 0.8 or 100 μmoles · min⁻¹ · 100 g⁻¹ adenosine with 0.1–5 mM glucose in the perfusion medium. It is concluded that adenosine does not affect directly the myocardial glucose carrier system, aerobic or anaerobic glucose breakdown or glycogenolysis, but enhances glucose uptake secondarily by increasing coronary flow. This interpretation is substantiated by the finding that mechanically produced increases in perfusion volume caused similar increases in myocardial glucose uptake as were observed with comparable adenosine-induced coronary flow increments.