Hassinen I E, Vuorinen K H, Ylitalo K, Ala-Rämi A
Department of Medical Biochemistry, University of Oulu, Finland.
Mol Cell Biochem. 1998 Jul;184(1-2):393-400.
A short period of ischemia followed by reperfusion produces a state of affairs in which the cells' potential for surviving longer ischemia is enhanced. This is called ischemic preconditioning. The effects of preconditioning are also related to the reperfusion damage which ensues upon tissue oxygenation. The role of the cellular energy state in reperfusion damage remains an enigma, although ischemic preconditioning is known to trigger mechanisms which contribute to the prevention of unnecessary ATP waste. In some species up to 80% of ATP hydrolysis in ischemia can be attributed to mitochondrial F1-F0-ATPase (ATP synthase), and a role for its inhibitor protein (IF1) in ATP preservation has been proposed. Although originally regarded as limited to large animals with a slow heart beat, inhibition by IF1 is probably a universal phenomenon. Coincidentally with ATPase inhibition, the decline in cellular ATP slows down, but even so the difference in ATP concentration between preconditioned and non-conditioned hearts is still small at the final stages of a long ischemia, when the beneficial effect of preconditioning is observable, although the energy state during reperfusion remains low in hearts which do not recover.
短时间缺血后再灌注会产生一种情况，即细胞在更长时间缺血中存活的潜力增强。这被称为缺血预处理。预处理的效果也与组织氧合后随之而来的再灌注损伤有关。尽管已知缺血预处理会触发有助于防止不必要的ATP浪费的机制，但细胞能量状态在再灌注损伤中的作用仍然是个谜。在某些物种中，缺血时高达80%的ATP水解可归因于线粒体F1-F0-ATP酶（ATP合酶），并且有人提出其抑制蛋白（IF1）在ATP保存中起作用。尽管最初认为仅限于心跳缓慢的大型动物，但IF1的抑制可能是一种普遍现象。与ATP酶抑制同时发生的是，细胞ATP的下降减缓，但即便如此，在长时间缺血的最后阶段，预处理心脏和未预处理心脏之间的ATP浓度差异仍然很小，此时预处理的有益效果是可观察到的，尽管在未恢复的心脏中再灌注期间的能量状态仍然很低。
