PHYSIOLOGICAL AND CLINICAL IMPLICATIONS OF MEDULLARY HYPOXIA
PHYSIOLOGICAL AND CLINICAL IMPLICATIONS OF MEDULLARY HYPOXIA
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DOI：
10.1111/j.1525-1594.1987.tb02711.x
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发表时间：
1987-12-01
影响因子：
2.4
通讯作者：
ROSEN, S
中科院分区：
文献类型：
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作者：
EPSTEIN, FH;BREZIS, M;ROSEN, S
由于逆流毛细血管流动，哺乳动物肾脏的肾髓质长期处于缺氧状态，环境氧张力徘徊在限制呼吸的临界po2附近。在这种环境下，髓质厚升肢（mTAL）富含线粒体的细胞需要大量的能量来完成离子运输的工作。因此，这些细胞特别容易受到缺氧损伤，正如在离体灌注大鼠肾脏的形态学变化所证明的那样。灌注肾的金属tal细胞缺氧损伤可因增加运输功的操作而大大加重，并可通过主动运输抑制剂（如瓦巴因或速尿）或阻断肾小球滤过来消除。实验性缺血损伤对主动转运的密切依赖表明，内源性转运抑制剂可能在调节髓质对健康和疾病缺氧损伤的易感性方面发挥重要的生理作用。这一作用的候选者包括腺苷和局部形成的ara - chidonic酸衍生物，它们已被证明影响代谢和运输。
Because of countercurrent capillary flow, the renal medulla of mammalian kidneys is perpetually hypoxic, the ambient oxygen tension hovering close to the critical Po2that limits respiration. Within this environment, the mitochondria‐rich cells of the medullary thick ascending limb (mTAL) require large amounts of energy to accomplish the work of ion transport. These cells are therefore uniquely vulnerable to anoxic damage, as is demonstrated by morphological changes in isolated perfused rat kidneys. The lesions of hypoxia in mTAL cells of perfused kidneys can be greatly exaggerated by maneuvers that increase the work of transport and practically eliminated by inhibitors of active transport, like ouabain or furosemide, or by interrupting glomerular filtration. The close dependence of experimental ischemic injury on active transport suggests that endogenous inhibitors of transport may play an important physiological role in modulating the susceptibility of the medulla to anoxic injury in health and disease. Candidates for this role include adenosine and locally formed derivatives of ara‐chidonic acid that have been shown to influence metabolism and transport.