Long-chain acyl-CoA and acylcarnitine hydrolase activities in normal and ischemic rabbit heart

Moore, Kathleen Healy; Bonema, John D.; Solomon, Flora

doi:10.1016/s0022-2828(84)80027-9

Cited by 8 publications

(1 citation statement)

References 28 publications

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“…The extent of accumulation of acylCoA and acylcarnitine during ischemia depends on several factors including the residual perfusion and the arterial fatty acid concentration [13,[20][21][22][23].…”

Section: Fatty Acid Metabolism During Acute Ischemiamentioning

confidence: 99%

Myocardial fatty acid oxidation during ischemia and reperfusion

et al. 1992

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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.

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Section: Fatty Acid Metabolism During Acute Ischemiamentioning

confidence: 99%