大鼠缺血性损伤后单个肾单位代偿性肥大。

W F Finn
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引用次数: 1

摘要

在Sprague-Dawley大鼠中,单肾细胞肾小球滤过率(SNGFR)的增加是由于肾小球血浆流量(GPF)的增加以及肾小球毛细血管超滤系数(Kf)的增加。当肾脏肿块因疾病或缺血性损伤而减少时,单个肾单位也会出现肥大。为了确定严重缺血损伤后恢复的少数肾单位SNGFR的影响因素,我们对单侧肾动脉完全闭塞1小时后4周的大鼠进行了研究,并将结果与正常大鼠进行比较。间接测定肾小球超滤动力学和微血管造影研究表明,尽管缺血后肾脏的肾总血流量减少,但少数肾单位是过度灌注的。这些肾细胞中GPF的增加以及Kf的显著增加是SNGFR增加的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Compensatory hypertrophy of single nephrons following ischemic injury in the rat.

In Sprague-Dawley rats, the increase in single nephron glomerular filtration rate (SNGFR) following uninephrectomy is due to an increase in glomerular plasma flow (GPF) along with an increase in the glomerular capillary ultrafiltration coefficient (Kf). Hypertrophy of individual nephrons also occurs when renal mass is reduced by disease or ischemic injury. To characterize the factors determining SNGFR in the minority of nephrons that recover from a severe ischemic insult, rats were studied 4 weeks after 1 hour of complete unilateral renal artery occlusion and the results compared to those obtained in normal rats. Indirect determination of the dynamics of glomerular ultrafiltration along with microangiographic studies indicated that despite a reduction in total renal blood flow in the postischemic kidney, a minority of nephrons were hyperperfused. The increase of GPF in these nephrons along with a significant increase in Kf was responsible for the observed increase in SNGFR.

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