RECOVERY FROM POST-ISCHEMIC ACUTE RENAL-FAILURE IN THE RAT

RECOVERY FROM POST-ISCHEMIC ACUTE RENAL-FAILURE IN THE RAT
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DOI:
10.1038/ki.1979.112
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发表时间:
1979-01-01
影响因子:
19.6
通讯作者:
CHEVALIER, RL
CHEVALIER, RL
中科院分区:
医学1区
文献类型:
--
作者:
FINN, WF;CHEVALIER, RL

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为了确定缺血后急性肾衰竭 (ARF) 的恢复模式,在大鼠单侧肾动脉完全闭塞 60 分钟后,每隔 1、2、4 和 8 周进行清除和微穿刺研究。 1 周时,缺血后肾脏的菊粉清除率 (CIn) 低于正常值的 2%。肾血流量(RBF)、停流(SFP)和估计肾小球毛细血管静水压(GCPe)的减少表明存在明显的肾小球前血管收缩。还有肾小管阻塞的证据。近端肾小管内压力(PITP)升高,体内和组织学切片上可见肾小管管型。 2 周时,CIn 增加了 10 倍以上。这种变化是在 RBF、SFP 或 GCPe 没有任何显着升高的情况下发生的。 PITP 已降至正常值,组织学切片显示肾小管管型程度显着减少。显微注射至近端回旋的3H-菊糖的同侧尿液回收已完成。在第 4 周和第 8 周,CIn 进一步但更逐渐增加,这与 RBF、SFP 和 GCPe 的逐渐增加相关。缺血后 ARF 的恢复以双相模式发生。 CIn 的最初升高与肾小管内梗阻的缓解相关,而随后 CIn 的升高与进行性肾血管舒张相关。
To define the pattern of recovery from postischemic acute renal failure (ARF), clearance and micropuncture studies were performed at intervals of 1, 2, 4 and 8 wk following 60 min of complete unilateral renal artery occlusion in the rat. At 1 wk, the inulin clearance (CIn) of the postischemic kidney was less than 2% of normal. The presence of marked preglomerular vasoconstriction was indicated by the reductions in renal blood flow (RBF), and stop-flow (SFP) and estimated glomerular capillary hydrostatic pressures (GCPe). There was also evidence of tubular obstruction. Proximal intratubular pressures (PITP) were elevated, and intratubular casts could be seen in vivo and on histologic sections. At 2 wk, CIn had increased more than 10-fold. This change occurred in the absence of any significant elevation in RBF, SFP or GCPe. PITP had fallen to normal values, and histologic sections revealed a marked reduction in the extent of intratubular casts. Ipsilateral urinary recovery of 3H-inulin microinjected into proximal convolutions was complete. At 4 and 8 wk, there were further but more gradual rises in CIn, which were associated with progressive increases in RBF, SFP and GCPe. Recovery from postischemic ARF occurred in a biphasic pattern. The initial rise in CIn was associated with the relief of intratubular obstruction, whereas subsequent rises in CIn occurred in association with progressive renal vasodilatation.