[Effect of experimental myocardial infarct on the rate of NADH and 3-hydroxybutyrate oxidation in heart mitochondria].
The rate of oxidation of NADH and 3-hydroxybutyrate was studied in heart mitochondria after short-term (60 min) occlusion of coronary artery and the subsequent reperfusion. Addition of NAD increased the rate of 3-hydroxybutyrate oxidation, lowered in mitochondria of impaired tissue, but no complete restoration occurred. Th 3-hydroxybutyrate dehydrogenase activity was decreased by 25%. The rate of NADH oxidation in ultrasonicated mitochondria from the infarction zone exceeded 2-fold the rate of 3-hydroxybutyrate oxidation. These data suggest that deficiency of NAD limited primarily the rate of 3-hydroxybutyrate oxidation in heart mitochondria under conditions of experimental myocardial infarction. The level of 3-hydroxybutyrate dehydrogenase activity appears to restrict the rate of 3-hydroxybutyrate oxidation after addition of NAD.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000818:Animals; D006884:Hydroxybutyrate Dehydrogenase / Q000378:metabolism; D006885:Hydroxybutyrates / Q000378:metabolism*; D066298:In Vitro Techniques; D008929:Mitochondria, Heart / Q000378:metabolism*; D009203:Myocardial Infarction / Q000378:metabolism*; D009243:NAD / Q000378:metabolism*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D011817:Rabbits
D006885:Hydroxybutyrates; D009243:NAD; D000244:Adenosine Diphosphate; D006884:Hydroxybutyrate Dehydrogenase
Vliianie éksperimental'nogo infarkta miokarda na skorost' okisleniia NADH i 3-oksibutirata v mitokhondriiakh serdtsa.