[Mechanism of ischemic disorders of fatty acid oxidation in heart mitochondria].
The article deals with the effect of permanent, temporal and total myocardial ischemia on the oxidation of acetate, hexanoate, palmitoylcarnitine and palmitoyl-CoA in isolated rabbit heart mitochondria. All the three models of ischemia in different experimental situations demonstrated a similar degree of fatty acid oxidation suppression independent of the length of acyl residue, the suppression being the greatest during the first hours and in total ischemia. Both in the control and in ischemia, respiratory activity was at its highest level with acetate, decreasing in the order above. Thus, the rate of Krebs' cycle reactions and of respiratory chain does not limit medium- and long-chain fatty acid oxidation. It is nevertheless established that suppression of their oxidation in ischemia is completely determined by the decrease of cytochrome S and of endogenous substrate intermediates of Krebs' cycle in the mitochondria; decreased adenine nucleotide and carnitine-palmitoyl-transferase transport (other authors' data) is not critical, at least in early ischemia (0.5 h). Ischemic mitochondria are characterized by incomplete palmitoylcarnitine oxidation.
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D000085:Acetates / Q000378:metabolism; D000818:Animals; D002208:Caproates / Q000378:metabolism; D002952:Citric Acid Cycle; D003327:Coronary Disease / Q000378:metabolism*; D003574:Cytochrome c Group / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism*; D066298:In Vitro Techniques; D008929:Mitochondria, Heart / Q000378:metabolism*; D010084:Oxidation-Reduction; D010171:Palmitoyl Coenzyme A / Q000378:metabolism; D010172:Palmitoylcarnitine / Q000378:metabolism; D011817:Rabbits
D000085:Acetates; D002208:Caproates; D003574:Cytochrome c Group; D005227:Fatty Acids; D010171:Palmitoyl Coenzyme A; D010172:Palmitoylcarnitine
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