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During permanent coronary artery occlusion (1 and 4 h) the respiratory rate of rabbit heart mitochondria with palmitoyl-CoA, palmitoyl carnitine and acetate was progressively reduced to a similar extent. Oxidation of palmitoyl carnitine was incomplete, whereas beta-oxidation of palmitoyl carnitine was not altered significantly. Postischemic reperfusion (3 h) promoted the recovery of mitochondrial respiration. The data obtained suggest that in both the control and ischemia, palmitate oxidation is limited by outer carnitine palmitoyltransferase but not limited by the tricarboxylic acid cycle and respiratory chain.
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