Myocardial glucose uptake and breakdown during adenosine-induced vasodilation.
In isolated K+ (16.2 mM)-arrested cat hearts perfused at constant pressure adenosine infusions (0.8 mumoles - min-1 - 100 g-1 for 10 min) caused an increase in myocardial 14C-glucose uptake and release of 14CO2 + H14CO3- AND 14C-lactate simultaneously with a rise in coronary flow. The ratio of the release of 14CO2 + H14CO3- to that of 14C-lactate and the specific activity of lactate in the effuate were not altered. In K+ -arrested hearts perfused with constant volume neither glucose uptake nor glucose breakdown were influenced by 0.8 or 100 mumoles - 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.
D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002199:Capillary Permeability / Q000187:drug effects; D002415:Cats; D003326:Coronary Circulation / Q000187:drug effects*; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*
D005947:Glucose; D000241:Adenosine