Schaper W, Vogt A, Htun P
Max-Planck-Institut, Abteilung für experimentelle Kardiologie, Bad Nauheim.
Z Kardiol. 1996;85 Suppl 6:185-90.
Repeated short coronary occlusions trigger probably more than one pathway leading to increased tolerance toward ischemia. Adenosine plays probably a very important but not an exclusive role. It may act via opening of A1-receptor-operated K(+)-channels that lead to hyperpolarization of the cell, and it has antiadrenergic actions. A proposed action of adenosine via protein kinase C is not confirmed. Trophic factors are expressed during short periods of ischemia and contribute to survival, probably via inhibition of apoptosis.
反复短暂的冠状动脉闭塞可能触发不止一条导致对缺血耐受性增加的途径。腺苷可能起着非常重要但并非唯一的作用。它可能通过打开A1受体操纵的钾通道发挥作用，该通道导致细胞超极化，并且它具有抗肾上腺素能作用。腺苷通过蛋白激酶C的拟议作用尚未得到证实。在短暂缺血期间会表达营养因子，可能通过抑制细胞凋亡来促进存活。
