Acute kidney injury (AKI) is a significant clinical problem associated with poor outcome. The kidney, due to its inhomogeneous blood flow, is particularly susceptible to changes in oxygen delivery and intrarenal hypoxia is a hallmark of AKI, and progression to chronic kidney disease. However, the role of intrarenal hypoxia per se in recovery from an ischemic insult is presently unclear. The present study was designed to investigate 1) the role of systemic hypoxia in the acute progression and recovery of AKI, and 2) if increased intrarenal oxygenation improves recovery from an ischemic insult. Anaesthetized male Sprague-Dawley rats were subjected to unilateral warm renal ischemia for 45 minutes followed by two hours of reperfusion under systemic hypoxia (10% inspired oxygen), normoxia (21% inspired oxygen), or hyperoxia (60% inspired oxygen). Intrarenal oxygen tension was successfully manipulated by altering the inspired oxygen. GFR prior to the ischemic insult was independent of intrarenal oxygen tension. GFR during the recovery from the ischemic insult was significantly lower compared to baseline in all groups (3±1, 13±1, and 30±11% of baseline for hypoxia, normoxia and hyperoxia, respectively). However, GFR was significantly higher in hyperoxia compared to hypoxia (P<0.05 hypoxia vs. hyperoxia). During the recovery, renal blood flow was only reduced in hyperoxia, as a consequence of increased renal vascular resistance. In conclusion, the present study demonstrates that renal function during the recovery from an ischemic insult is dependent on intrarenal oxygen availability, and normobaric hyperoxia treatment has the potential to protect kidney function.

中文翻译：

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肾内氧合决定缺血性损伤恢复期间的肾功能

急性肾损伤（AKI）是与不良预后相关的重大临床问题。肾脏由于其血流不均匀而特别容易发生氧气输送的变化，而肾内缺氧是AKI的标志，并发展为慢性肾脏疾病。然而，目前尚不清楚肾内低氧本身在缺血性损伤恢复中的作用。本研究旨在研究1）全身性缺氧在AKI急性进展和恢复中的作用，以及2）肾内氧合增加是否改善缺血性损伤的恢复。麻醉的雄性Sprague-Dawley大鼠在系统性缺氧（10％吸入氧气），常氧（21％吸入氧气）或高氧（60％吸入氧气）下进行单侧温暖肾缺血45分钟，然后再灌注2小时。通过改变吸入的氧气成功地控制了肾内氧气的张力。缺血性损伤之前的GFR与肾内氧张力无关。在所有组中，缺血性损伤恢复期间的GFR均明显低于基线（低氧，常氧和高氧分别为基线的3±1、13±1和30±11％）。然而，与低氧相比，高氧时的GFR明显更高（与高氧相比P <0.05低氧）。在恢复过程中，仅在高氧状态下肾血流量减少，这是肾血管阻力增加的结果。总之，本研究表明缺血性损伤恢复过程中的肾功能取决于肾内氧的可用性，而常压高氧治疗具有保护肾功能的潜力。