BULK ISOLATION OF RENAL PCT AND PST .2. DIFFERENTIAL RESPONSES TO ANOXIA OR HYPOXIA
BULK ISOLATION OF RENAL PCT AND PST .2. DIFFERENTIAL RESPONSES TO ANOXIA OR HYPOXIA
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DOI：
10.1152/ajprenal.1990.259.1.f176
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发表时间：
1990-07-01
影响因子：
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通讯作者：
MANDEL, LJ
中科院分区：
文献类型：
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作者：
RUEGG, CE;MANDEL, LJ
本实验通过观察缺氧或低氧对离体兔肾近曲段（PCT）和直段（PST）固有生化反应的影响，探讨了肾段选择性损伤的机制。大量分离后，将富含PCT或PST的悬浮液（1 mg/ml）在Dulbecco改良的Spille-s-Hams F-12培养基中预孵育1 h，然后暴露于缺氧（N2）40 min或缺氧（1% O2）120 min，并在空气-CO2条件下恢复1 h。从缺氧状态恢复后，PCT和PST中各活力指标的对照值百分比分别如下：耗氧量（Qo 2），30/50; ATP含量，22/49; K+含量，60.70 ;乳酸脱氢酶（LDH）释放百分比，66/45。同样，从缺氧恢复后，PCT和PST的对照值百分比分别如下：O2消耗（Qo 2），30/50; ATP含量，22/49; K+含量，60/70;乳酸脱氢酶（LDH）释放百分比，66/45。同样，从缺氧恢复后，PCT和PST的对照值百分比分别如下：Qo 2; 50/90; ATP，16/57; K+，52/79; LDH，45/17。这些不同的反应表明，PCT段先天更容易受到缺氧和缺氧损伤比PST段。由于ATP含量显着较高的PST段后立即缺氧和缺氧，我们研究了葡萄糖依赖性反应在缺氧暴露这些段缺氧30分钟的营养缓冲液中有或没有葡萄糖。这些实验的结果表明，PST对缺氧的保护是葡萄糖依赖性的，因为在缺氧期间从营养缓冲液中去除葡萄糖消除了PCT和PST之间的差异反应。这里观察到的体外PCT敏感性与体内缺血后观察到的PST敏感性形成对比，表明体内存在的血液动力学因素可能最终决定原位PST节段的总体敏感性。
Innate biochemical responses of rabbit renal proximal convoluted (PCT) and straight (PST) segments following in vitro exposure to anoxia or hypoxia were investigated to delineate the mechanisms responsible for segment-selective injury in vivo. After bulk isolation, suspension (1 mg/ml) enriched in either PCT or PST were preincubated in Dulbecco''s modified Eagle-s-Ham''s F-12 medium for 1-h before being exposed to either 40 min of anoxia (N2) or 120 min of hypoxia (1% O2) and 1 h of recovery under air-CO2 conditions. After recovery from anoxia, the percent of control values for each viability indicator in PCT and PST, respectively, were as follows: O2 consumption (Qo2), 30/50; ATP content , 22/49; K+ content, 60.70 ; and percent lactate dehydrogenase (LDH) release, 66/45. Likewise, following recovery from hypoxia, the percent of control values for PCT and PST, respectively, were as follows: O2 consumption (Qo2), 30/50; ATP content, 22/49; K+ content, 60/70; and percent lactate dehydrogenase (LDH) release, 66/45. Likewise, following recovery from hypoxia, the percent of control values for PCT and PST, respectively, were as follows: Qo2; 50/90; ATP, 16/57; K+, 52/79; LDH, 45/17. These differential responses indicate that PCT segments were innately more susceptible to anoxic and hypoxic injury than PST segments. Because ATP content was significantly higher in PST segments immediately after anoxia and hypoxia, we investigated glucose-dependent responses during anoxia by exposing these segments to 30 min of anoxia in nutrient buffer with or without glucose. Results from these experiments demonstrate that the PST protection from anoxia was glucose dependent because removal of glucose from the nutrient buffers during anoxia abolishes the differential responses between PCT and PST. The in vitro PCT sensitivity observed here contrasts with the PST sensitivity observed following in vivo ischemia, suggesting that hemodynamic factors present in vivo may ultimately determine the overall susceptibility of PST segments in situ.