Dzheia P P, Toleĭkis A I, Prashkiavichius A K
Vopr Med Khim. 1980 Sep-Oct;26(5):591-4.
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. The 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.
在冠状动脉短期（60分钟）闭塞并随后再灌注后，研究了心脏线粒体中NADH和3-羟基丁酸的氧化速率。添加NAD可提高3-羟基丁酸的氧化速率，该速率在受损组织的线粒体中降低，但未完全恢复。3-羟基丁酸脱氢酶活性降低了25%。梗死区超声处理的线粒体中NADH的氧化速率超过3-羟基丁酸氧化速率的2倍。这些数据表明，在实验性心肌梗死的情况下，NAD的缺乏主要限制了心脏线粒体中3-羟基丁酸的氧化速率。添加NAD后，3-羟基丁酸脱氢酶活性水平似乎限制了3-羟基丁酸的氧化速率。
