Brezis M, Rosen S, Spokes K, Silva P, Epstein F H
Am J Pathol. 1984 Aug;116(2):327-41.
The hypothesis that decrease in energy demand may prevent anoxic cell damage has been examined in the medullary thick ascending limb of isolated perfused rat kidneys exposed to oxygen deprivation. The effects of decreasing active reabsorptive transport in the medullary thick ascending limb were observed on the extensive damage regularly induced by hypoxic perfusion (gassed with no oxygen) or potassium cyanide. Anoxic injury was consistently attenuated or abolished if reabsorptive transport was decreased with ouabain or furosemide or by halting the glomerular filtration rate with the use of a hyperoncotic medium (nonfiltering kidney). Comparison of the injury generated by warm ischemia for identical time periods showed that complete ischemia does not reproduce the severe lesions seen during hypoxic perfusion. These results suggest that transport activity is a determining factor of anoxic cell death in the thick ascending limb of Henle's loop.
能量需求降低可能预防缺氧性细胞损伤这一假说，已在暴露于缺氧环境的离体灌注大鼠肾脏的髓袢升支粗段中进行了研究。观察了髓袢升支粗段主动重吸收转运减少对缺氧灌注（用无氧气体通气）或氰化钾 regularly 诱导的广泛损伤的影响。如果用哇巴因或呋塞米降低重吸收转运，或使用高渗介质（无滤过肾）停止肾小球滤过率，缺氧损伤会持续减轻或消除。相同时间段内温缺血产生的损伤比较表明，完全缺血不会重现缺氧灌注期间所见的严重病变。这些结果表明，转运活性是亨氏袢升支粗段缺氧性细胞死亡的决定因素。
