Bittar N, Shug A L, Folts J D, Koke J R
Recent Adv Stud Cardiac Struct Metab. 1976;12:167-74.
Experiments were conducted in two canine models. Intracoronary infusion of atractyloside resulted in physiological, biochemical, and ultrastructural changes similar to those seen with ischemia. The fact that atractyloside, a specific inhibitor of adenine nucleotide translocase produces this change in vivo suggests that this inhibition in the key disturbance that initiates the metabolic derangements seen with ischemia. This chemical model seems to provide unique opportunities to study the possible factors that may reverse adenine nucleotide translocase inhibition and thus possibly prevent cell injury.
实验在两种犬类模型中进行。冠状动脉内输注苍术苷会导致生理、生化和超微结构变化，这些变化与缺血时所见的变化相似。腺嘌呤核苷酸转位酶的特异性抑制剂苍术苷在体内产生这种变化这一事实表明，这种抑制作用是引发缺血时所见代谢紊乱的关键干扰因素。这种化学模型似乎为研究可能逆转腺嘌呤核苷酸转位酶抑制作用从而可能预防细胞损伤的潜在因素提供了独特的机会。
