Lipid and glycogen metabolism in the hypoxic heart: effects of epinephrine.
The metabolism of cardiac lipids and glycogen in hypoxic and well-oxygenated perfused rat hearts was studied in the presence or absence of epinephrine. Heart lipids were pre-labeled in vivo with [1-14C]palmitate. Triglyceride disappearance (measured chemically and radiochemically) was observed in well-oxygenated hearts and was stimulated by epinephrine (4.1 X 10(-7)M). Utilization of tissue triglycerides was inhibited in hypoxic hearts in the presence or absence of added epinephrine. Hypoxia resulted in a small increase in tissue 14C-free fatty acids and inhibition of 14C-labeled triglyceride fatty acid oxidation. Epinephrine had no stimulatory effect on fatty acid oxidation in hypoxic hearts. Utilization of 14C-labeled phospholipids (and total phospholipids) was similar in well-oxygenated and hypoxic hearts with or without added epinephrine. These results suggested that the antilipolytic effects of hypoxia were predominant over the lipolytic effects of epinephrine. Glycogenolysis was stimulated threefold by epinephrine in well-oxygenated hearts. Hypoxia alone was a potent stimulus to glycogenolysis. Addition of epinephrine to perfusates of hypoxic hearts resulted in a slight enhancement of glycogenolysis.
D000818:Animals; D002245:Carbon Dioxide / Q000096:biosynthesis; D004837:Epinephrine / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005947:Glucose / Q000096:biosynthesis; D006003:Glycogen / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism*; D050356:Lipid Metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D010477:Perfusion / Q000379:methods; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D014280:Triglycerides / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D010743:Phospholipids; D014280:Triglycerides; D002245:Carbon Dioxide; D006003:Glycogen; D005947:Glucose; D004837:Epinephrine