Bosetti F, Yu G, Zucchi R, Ronca-Testoni S, Solaini G
Scuola Superiore di Studi Universitari e di Perfezionamento S. Anna, Pisa, Italy.
Mol Cell Biochem. 2000 Dec;215(1-2):31-7. doi: 10.1023/a:1026558922596.
A short period of ischemia followed by reperfusion (ischemic preconditioning) is known to trigger mechanisms that contribute to the prevention of ATP depletion. In ischemic conditions, most of the ATP hydrolysis can be attributed to mitochondrial F1F0-ATPase (ATP synthase). The purpose of the present study was to examine the effect of myocardial ischemic preconditioning on the kinetics of ATP hydrolysis by F1F0-ATPase. Preconditioning was accomplished by three 3-min periods of global ischemia separated by 3 min of reperfusion. Steady state ATP hydrolysis rates in both control and preconditioned mitochondria were not significantly different. This suggests that a large influence of the enzyme on the preconditioning mechanism may be excluded. However, the time required by the reaction to reach the steady state rate was increased in the preconditioned group before sustained ischemia, and it was even more enhanced in the first 5 min of reperfusion (101 +/- 3.0 sec in preconditioned vs. 83.4 +/- 4.4 sec in controls, p < 0.05). These results suggest that this transient increase in activation time may contribute to the cardioprotection by slowing the ATP depletion in the very critical early phase of post-ischemic reperfusion.
已知短时间缺血后再灌注（缺血预处理）会触发有助于防止ATP耗竭的机制。在缺血条件下，大部分ATP水解可归因于线粒体F1F0 - ATP酶（ATP合酶）。本研究的目的是研究心肌缺血预处理对F1F0 - ATP酶ATP水解动力学的影响。预处理通过三个3分钟的全心缺血期并间隔3分钟再灌注来完成。对照线粒体和预处理线粒体的稳态ATP水解速率无显著差异。这表明该酶对预处理机制的重大影响可能被排除。然而，在持续缺血前，预处理组中反应达到稳态速率所需的时间增加，并且在再灌注的前5分钟内进一步延长（预处理组为101±3.0秒，对照组为83.4±4.4秒，p<0.05）。这些结果表明，这种激活时间的短暂增加可能通过在缺血后再灌注的非常关键的早期阶段减缓ATP耗竭而有助于心脏保护。
