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肾质量减少后侏儒大鼠的肾功能和形态学

Renal function and morphometry in the dwarf rat following a reduction in renal mass.

作者信息

Haylor J, Chowdry J, Baillie H, Cope G, el Nahas A M

机构信息

Sheffield Kidney Institute, Northern General Hospital, UK.

出版信息

Nephrol Dial Transplant. 1996 Apr;11(4):643-50. doi: 10.1093/oxfordjournals.ndt.a027353.

Abstract

BACKGROUND

The compensatory increase in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) which follows a reduction in renal mass may be mediated by growth hormone, a renal vasodilator.

METHODS

GFR, ERPF and glomerular morphometry were assessed in the dwarf rat, selectively deficient in GH, and compared its Lewis base strain. Studies were performed 21-days after sham-operation, unilateral nephrectomy or subtotal nephrectomy in age-matched animals. GFR and ERPF were assessed from the renal clearance of inulin and p-aminohippurate measured under barbiturate anaesthesia.

RESULTS

The dwarf rat had a lower GFR and ERPF than the Lewis rat, in proportion to its lower body weight and lower kidney weight. Kidneys from the dwarf rat had a similar number of glomeruli to the Lewis, but smaller glomerular components in proportion to a lower kidney weight. Following unilateral nephrectomy, GFR (dwarf + 58%, Lewis + 53%) and ERPF (dwarf + 58%, Lewis + 52%) increased to a similar degree in both rat strains. Glomerular diameter, volume and capillary surface area increased in proportion to kidney growth, although compensatory renal growth (dwarf + 62%, Lewis + 78%) was somewhat lower in the dwarf. Following 5/6 subtotal nephrectomy, GFR (dwarf + 143%, Lewis + 171%) increased to a similar degree in both rat strains while ERPF (dwarf + 108%, Lewis + 48%) and compensatory renal growth (dwarf + 115%, Lewis + 86%) were greater in the dwarf than the Lewis rat. Subtotal nephrectomy was also associated with an increase in the thickness of the glomerular basement membrane in both rat strains.

CONCLUSIONS

The results do not support a role for GH in the compensatory increase in renal function or hypertrophy which follows a reduction in renal mass, excluding this as a potential mechanism for GH-dependent renal scarring.

摘要

背景

肾质量减少后肾小球滤过率(GFR)和有效肾血浆流量(ERPF)的代偿性增加可能由生长激素介导,生长激素是一种肾血管扩张剂。

方法

评估生长激素选择性缺乏的侏儒大鼠的GFR、ERPF和肾小球形态,并与Lewis品系大鼠进行比较。在年龄匹配的动物中,于假手术、单侧肾切除或次全肾切除21天后进行研究。在巴比妥类麻醉下,通过菊粉和对氨基马尿酸的肾清除率评估GFR和ERPF。

结果

侏儒大鼠的GFR和ERPF低于Lewis大鼠,与其较低的体重和肾重成比例。侏儒大鼠的肾脏肾小球数量与Lewis大鼠相似,但与较低的肾重成比例,其肾小球成分较小。单侧肾切除后,两种品系大鼠的GFR(侏儒大鼠增加58%,Lewis大鼠增加53%)和ERPF(侏儒大鼠增加58%,Lewis大鼠增加52%)增加程度相似。肾小球直径、体积和毛细血管表面积随肾脏生长而增加,尽管侏儒大鼠的代偿性肾脏生长(侏儒大鼠增加62%,Lewis大鼠增加78%)略低。5/6次全肾切除后,两种品系大鼠的GFR(侏儒大鼠增加143%,Lewis大鼠增加171%)增加程度相似,而侏儒大鼠的ERPF(侏儒大鼠增加108%,Lewis大鼠增加48%)和代偿性肾脏生长(侏儒大鼠增加115%,Lewis大鼠增加86%)比Lewis大鼠更大。次全肾切除还与两种品系大鼠肾小球基底膜厚度增加有关。

结论

结果不支持生长激素在肾质量减少后肾功能代偿性增加或肥大中起作用,排除了其作为生长激素依赖性肾瘢痕形成潜在机制的可能性。

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