Department of Science, Institute of Pharmacology, University of Pavia, Italy.
Biochem Pharmacol. 1981 Sep 1;30(17):2399-408. doi: 10.1016/0006-2952(81)90333-6.
Changes in the maximal rate of some cerebral enzymatic activities related to energy transduction (lactate dehydrogenase; citrate synthase and malate dehydrogenase; total NADH-cytochrome c reductase and cytochrome oxidase) as well as both glutamate dehydrogenase and acetylcholine esterase were assayed in the purified mitochondrial fraction or in crude synaptosomal fraction from cerebral cortex. The evaluations were performed in rats before and after a postdecapitative normothermic ischemia of 5, 10, 20 and 40 min duration. The ischemic damage resulted in a decrease in the activity of mitochondrial malate dehydrogenase and total NADH-cytochrome c reductase, and of synaptosomal acetylcholine esterase. The biochemical evaluations were performed also after an i.p. pretreatment with vincamine, trimetazidine and suloctidil (50 mg/kg). The drugs induced different changes in enzyme activities as a function of the ischemia duration. These various interferences are discussed with regard to the possible drugs mode of action.
在纯化的线粒体部分或皮质的粗突触体部分中测定了与能量转导相关的一些脑酶最大速率的变化(乳酸脱氢酶;柠檬酸合酶和苹果酸脱氢酶;总 NADH-细胞色素 c 还原酶和细胞色素氧化酶),以及谷氨酸脱氢酶和乙酰胆碱酯酶。在断头后进行 5、10、20 和 40 分钟的常温缺血之前和之后,在大鼠中进行了评估。缺血损伤导致线粒体苹果酸脱氢酶和总 NADH-细胞色素 c 还原酶以及突触体乙酰胆碱酯酶活性降低。还在腹腔内用长春胺、曲美他嗪和舒洛地尔(50mg/kg)预处理后进行了生化评估。这些药物根据缺血持续时间引起了不同的酶活性变化。这些各种干扰与可能的药物作用模式有关进行了讨论。