Brezis M, Rosen S, Silva P, Spokes K, Epstein F H
Experientia. 1986 May 15;42(5):570-2. doi: 10.1007/BF01946708.
In brain, heart and kidney, cell work in the absence of oxygen has been thought to precipitate anoxic damage by increasing the rate of depletion of cellular energy stores. In the medullary thick ascending limb of isolated perfused rat kidneys, however, reduction of ATP synthesis by a variety of mitochondrial or metabolic inhibitors caused ATP depletion comparable to that produced by oxygen deprivation but did not reproduce the lesions of anoxia. In these cells, unrestrained mitochondrial activity may be an important source of anoxic injury.
在脑、心脏和肾脏中，人们一直认为细胞在无氧状态下的工作会通过加快细胞能量储备的消耗速度而引发缺氧损伤。然而，在分离灌注的大鼠肾脏的髓质厚升支中，多种线粒体或代谢抑制剂导致的ATP合成减少所引起的ATP耗竭与缺氧所产生的ATP耗竭相当，但并未重现缺氧损伤。在这些细胞中，不受抑制的线粒体活动可能是缺氧损伤的一个重要来源。
