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首页> 外文期刊>American Journal of Physiology >Renal ischemic injury results in permanent damage to peritubular capillaries and influences long-term function.
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Renal ischemic injury results in permanent damage to peritubular capillaries and influences long-term function.

机译：肾脏缺血性损伤会导致肾小管周围毛细血管永久性损害，并影响长期功能。

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Acute episodes of severe renal ischemia result in acute renal failure (ARF). These episodes are followed by a characteristic recovery and repair response, whereby tubular morphology and renal function appear completely restored within approximately 1 mo. However, the chronic effects of such an injury have not been well studied. Male rats were subjected to 60-min bilateral ischemia followed by reperfusion, yielding a characteristic injury. Postischemic animals manifested severe diuresis, peaking at 1 wk postinjury (volume: >45 ml/day, ARF vs. 18 ml/day, sham; P < 0.05). Urine flow subsequently declined but remained significantly elevated vs. sham animals for a 40-wk period. The prolonged alteration in urinary concentrating ability was attributable, in part, to a diminished capacity to generate a hypertonic medullary interstitium. By week 16, proteinuria developed in the post-ARF group and progressed for the duration of the study. Histological examination revealed essentially normal tubular morphology at4 and 8 wk postinjury but the development of tubulointerstitial fibrosis at 40 wk. Transforming growth factor (TGF)-beta1 expression was elevated at 40 wk, but not at 4 and 8 wk postinjury. Microfil analysis revealed an approximately 30-50% reduction in peritubular capillary density in the inner stripe of the outer medulla at 4, 8, and 40 wk in post-ARF groups vs. sham animals. In addition, post-ARF rats manifested a significant pressor response to a low dose of ANG II (15 ng x kg(-1) x min(-1)). We hypothesize that severe ischemic injury results in a permanent alteration of renal capillary density, contributing to a urinary concentrating defect and the predisposition toward the development of renal fibrosis.
机译：严重的肾脏缺血的急性发作会导致急性肾衰竭（ARF）。这些发作后会出现特征性的恢复和修复反应，从而使肾小管形态和肾功能在大约1 mo内完全恢复。但是，这种损伤的慢性影响尚未得到很好的研究。对雄性大鼠进行60分钟的双侧缺血，然后再灌注，产生特征性损伤。缺血后的动物表现出严重的利尿作用，在受伤后第1周达到峰值（体积：> 45 ml /天，ARF与18 ml /天，假; P <0.05）。随后尿液流量下降，但与假动物相比，在40周内尿液流量仍显着升高。尿液浓缩能力的长期改变部分归因于产生高渗性髓质间质的能力降低。到第16周时，蛋白尿在ARF后组中发展，并在研究期间进展。组织学检查显示在损伤后第4周和第8周基本上呈正常的肾小管形态，但在第40周时肾小管间质纤维化发展。受伤后40周时转化生长因子（TGF）-β1表达升高，但在伤后4周和8周时均未升高。 Microfil分析显示，与假手术组相比，ARF后组在第4、8和40周时，延髓内条纹的肾小管周毛细血管密度降低了约30-50％。此外，ARF后大鼠对低剂量的ANG II（15 ng x kg（-1）x min（-1））表现出明显的升压反应。我们假设严重的缺血性损伤会导致肾毛细血管密度的永久性改变，从而导致尿液浓缩缺陷和易患肾纤维化的倾向。

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