Wahlberg J
Scand J Urol Nephrol Suppl. 1983;73:1-30.
The renal pathophysiology during ureteral obstruction was investigated in rat experiments, especially designed to study the role of the tubuloglomerular feedback (TGF) control mechanism. This mechanism, operating by sensing the distal delivery of fluid to the macula densa site, regulates the glomerular capillary pressure (PGC) and the glomerular filtration rate (GFR). Interstitial pressure conditions are known to influence the sensitivity of this control mechanism. Micropuncture experiments were performed to investigate the TGF activity before, during and after release of 2 h unilateral ureteral obstruction (UUO) and after 24 h UUO and bilateral ureteral obstruction (BUO). Renal interstitial hydrostatic and oncotic pressure, proximal stop-flow pressure (PSF) and GFR were also determined. In other experiments, the effects of indomethacin on renal pelvic pressure and PGC, estimated from PSF, were studied during the initial vasodilatory phase of UUO. Cortical and regional medullary blood flow was measured using a combination of labelled microspheres and the 86-Rb extraction method. The present results indicate that the initial vasodilatation, demonstrated by an increased PGC and accompanied by an elevated renal pelvic pressure, was caused by prostaglandin release. These pressures could be reduced by injection of indomethacin. Blood flow measurements revealed that the initial vasodilatation seems to occur both in the cortex and in the medulla, but after a few hours progressive vasoconstriction took place in all regions of the kidney. Two hours of UUO caused increased interstitial hydrostatic and decreased oncotic pressure and the TGF response was abolished. This phenomenon participated in the vasodilatory process at this stage of UUO. After release of 2 h UUO, GFR was reduced, indicating vasoconstriction, probably caused by activation of the highly sensitized TGF control mechanism seen in this situation. At 24 h of UUO there was a normal hydrostatic and high oncotic pressure and high TGF sensitivity. These findings contrast to those at 24 h of BUO, with normal interstitial pressure conditions and a slight decrease in TGF sensitivity. These differences between animals with UUO and BUO might be of importance for the absence of post-obstructive diuresis in UUO and the presence of this phenomenon in BUO animals.
在大鼠实验中研究了输尿管梗阻期间的肾脏病理生理学，这些实验特别设计用于研究肾小管-肾小球反馈（TGF）控制机制的作用。该机制通过感知液体向致密斑部位的远端输送来运作，调节肾小球毛细血管压力（PGC）和肾小球滤过率（GFR）。已知间质压力状况会影响这种控制机制的敏感性。进行了微穿刺实验，以研究单侧输尿管梗阻（UUO）2小时解除前、解除期间和解除后以及UUO 24小时和双侧输尿管梗阻（BUO）后TGF的活性。还测定了肾间质静水压和胶体渗透压、近端停流压力（PSF）和GFR。在其他实验中，研究了吲哚美辛在UUO初始血管舒张期对肾盂压力和根据PSF估算的PGC的影响。使用标记微球和86-Rb提取法相结合的方法测量皮质和局部髓质血流。目前的结果表明，PGC升高所显示的初始血管舒张并伴有肾盂压力升高是由前列腺素释放引起的。注射吲哚美辛可降低这些压力。血流测量显示，初始血管舒张似乎在皮质和髓质中均会发生，但数小时后肾脏所有区域均出现进行性血管收缩。UUO 2小时导致间质静水压升高和胶体渗透压降低，TGF反应消失。这种现象参与了UUO此阶段的血管舒张过程。UUO 2小时解除后，GFR降低，表明血管收缩，这可能是由在这种情况下所见的高度敏感的TGF控制机制激活所致。UUO 24小时时，静水压正常，胶体渗透压高，TGF敏感性高。这些发现与BUO 24小时时的情况形成对比，此时间质压力状况正常，TGF敏感性略有降低。UUO和BUO动物之间的这些差异可能对UUO中无梗阻后利尿以及BUO动物中存在这种现象具有重要意义。
