Jensen P K, Steven K, Blaehr H, Christiansen J S, Parving H H
Kidney Int. 1986 Feb;29(2):490-5. doi: 10.1038/ki.1986.26.
The glomerular hemodynamics were studied in streptozotocin diabetic rats 3 months after the induction and in age-matched normal animals. Indomethacin infusion failed to cause changes in glomerular hemodynamics in normal rats but produced striking effects in the diabetic rats: The afferent arteriolar hydraulic resistance increased substantially while the efferent resistance rose moderately causing large reductions in single nephron blood flow and in the hydraulic pressure in the glomerular capillaries. Consequently, single nephron glomerular filtration rate (SNGFR) was reduced significantly below normal. The ultrafiltration coefficient of the glomerular membrane was significantly lower in the diabetic than in the normal animals (2.8 versus 5.0 nl min-1 mm Hg-1) and remained unchanged during indomethacin infusion. Our results suggest that the prostaglandin system compensates for the changes in the glomerular hemodynamics induced by diabetes by reducing the arteriolar resistances to increase the glomerular capillary pressure making it possible to maintain normal values of SNGFR and nephron blood flow.
在链脲佐菌素诱导糖尿病3个月后的大鼠以及年龄匹配的正常动物中研究了肾小球血流动力学。在正常大鼠中，输注吲哚美辛未能引起肾小球血流动力学变化，但在糖尿病大鼠中产生了显著影响：入球小动脉水力阻力大幅增加，而出球小动脉阻力适度升高，导致单个肾单位血流量和肾小球毛细血管液压大幅降低。因此，单个肾单位肾小球滤过率（SNGFR）显著低于正常水平。糖尿病大鼠肾小球膜超滤系数显著低于正常动物（2.8对5.0 nl min-1 mm Hg-1），且在输注吲哚美辛期间保持不变。我们的结果表明，前列腺素系统通过降低小动脉阻力以增加肾小球毛细血管压力来补偿糖尿病诱导的肾小球血流动力学变化，从而有可能维持SNGFR和肾单位血流量的正常值。
