Myocardial fatty acid oxidation during ischemia and reperfusion.
Inhibition of fatty acid oxidation is an early event in myocardial ischemia that most likely contributes to tissue injury by the accumulation of potentially toxic intermediates such as acylCoA and acylcarnitine. After reperfusion both myocardial oxygen consumption and fatty acid oxidation may rapidly recover to preischemic levels, even when contractile function remains depressed. The mechanisms underlying the apparent dissociation between contractile function and oxidative metabolism early during reperfusion are still controversial. In isolated rat hearts subjected to 60 min of no-flow ischemia myocardial oxygen consumption and oxidation of palmitate were lowered during reperfusion by 3 mM of NiCl2 and by 6 microM of ruthenium red. The results provide indirect evidence for the hypothesis that intracellular calcium transport may be involved in the mechanisms responsible for the high oxidative metabolic rate early after reperfusion.
D000208:Acute Disease; D000818:Animals; D002118:Calcium / Q000502:physiology*; D004285:Dogs; D004734:Energy Metabolism; D005227:Fatty Acids / Q000378:metabolism*; D008929:Mitochondria, Heart / Q000378:metabolism; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009532:Nickel / Q000494:pharmacology; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D010168:Palmitates / Q000378:metabolism; D051381:Rats; D012430:Ruthenium Red / Q000494:pharmacology
D005227:Fatty Acids; D010168:Palmitates; D012430:Ruthenium Red; C022838:nickel chloride; D009532:Nickel; D002118:Calcium