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底物可诱导离体大鼠肾脏髓袢升支粗段发生缺氧性损伤。

Substrates induce hypoxic injury to medullary thick limbs of isolated rat kidneys.

作者信息

Brezis M, Rosen S, Spokes K, Silva P, Epstein F H

出版信息

Am J Physiol. 1986 Oct;251(4 Pt 2):F710-7. doi: 10.1152/ajprenal.1986.251.4.F710.

DOI:10.1152/ajprenal.1986.251.4.F710
PMID:3766745
Abstract

Under certain conditions, excess of substrates may be detrimental to the kidney. In isolated rat kidneys perfused with cell-free medium, oxidative metabolism to support reabsorptive transport in the presence of a limited oxygen supply results in hypoxic injury to medullary thick ascending limbs (mTAL). Since inhibitors of mitochondrial respiration markedly reduced this injury, we evaluated the effects of altering the availability of substrate for oxidative metabolism in the mTAL. Inhibition of glucose utilization with 2-deoxyglucose (50 mM) and simultaneous inhibition of long-chain fatty acid metabolism with 2-tetradecylglycidic acid (10(-4) M) in the absence of exogenous substrates consistently reduced hypoxic cell injury to mTAL. Similarly, the direct inhibition of substrate oxidation by the citric acid cycle with monofluoroacetate (5 mM) also reduced the extent of damage to this nephron segment. Bypassing these metabolic blockades with L-lactate, pyruvate, or alpha-ketoglutarate stimulated renal oxidative metabolism and increased hypoxic damage to mTAL. Enhanced renal metabolism and function (higher renal oxygen consumption, tubular reabsorption of sodium, and glomerular filtration rate) were paradoxically associated with greater damage to mTAL. Thus, when oxygen supply is limited, substrate-supported aerobic metabolic activity for tubular transport may induce hypoxic injury in the renal medulla.

摘要

在某些情况下,底物过量可能对肾脏有害。在灌注无细胞培养基的离体大鼠肾脏中,在氧气供应有限的情况下,为支持重吸收转运的氧化代谢会导致髓质厚升支(mTAL)发生缺氧损伤。由于线粒体呼吸抑制剂能显著减轻这种损伤,我们评估了改变mTAL中氧化代谢底物可用性的影响。在没有外源底物的情况下,用2-脱氧葡萄糖(50 mM)抑制葡萄糖利用,并同时用2-十四烷基甘油酸(10^(-4) M)抑制长链脂肪酸代谢,持续减轻了mTAL的缺氧细胞损伤。同样,用单氟乙酸(5 mM)直接抑制柠檬酸循环的底物氧化也减少了该肾单位节段的损伤程度。用L-乳酸、丙酮酸或α-酮戊二酸绕过这些代谢障碍会刺激肾脏氧化代谢,并增加mTAL的缺氧损伤。增强的肾脏代谢和功能(更高的肾脏耗氧量、肾小管对钠的重吸收以及肾小球滤过率)与mTAL更大的损伤自相矛盾地相关。因此,当氧气供应有限时,底物支持的肾小管转运有氧代谢活动可能会在肾髓质中诱导缺氧损伤。

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