Sjödin J G, Wahlberg J, Persson A E
J Urol. 1982 May;127(5):1017-20. doi: 10.1016/s0022-5347(17)54178-6.
The present investigation was undertaken to determine whether elevated glomerular capillary and pelvic pressure resulting from ureteral obstruction could be lowered by injection of indomethacin. In hydropenic rats and rats subjected to saline volume expansion, the mean arterial blood pressure, renal pelvic pressure and proximal tubular free flow and stop-flow pressures were measured during acute ureteral obstruction. Indomethacin was injected intravenously 30 to 45 minutes after obstruction at a renal pelvic pressure of 35 mm. Hg or higher. In the former group of rats the proximal tubular stop-flow pressure decreased by an average of 32 per cent and renal pelvic pressure by 27 per cent on administration of indomethacin, whereas in the volume expanded rats (saline, 2 per cent of body weight) these pressures did not change significantly. These results suggest that the vasodilation consequent to ureteral obstruction in hydropenic animals is caused by prostaglandins release and can be abolished by indomethacin, whereas the vasodilation that results from ureteral obstruction in volume expanded animals may be affected by additional mechanisms.
本研究旨在确定输尿管梗阻导致的肾小球毛细血管和肾盂压力升高是否可通过注射吲哚美辛降低。在缺水大鼠和进行生理盐水容量扩张的大鼠中，在急性输尿管梗阻期间测量平均动脉血压、肾盂压力、近端肾小管自由流和停流压力。在梗阻后30至45分钟，当肾盂压力达到35毫米汞柱或更高时静脉注射吲哚美辛。在缺水大鼠组中，给予吲哚美辛后近端肾小管停流压力平均降低32%，肾盂压力降低27%，而在容量扩张大鼠（生理盐水，体重的2%）中，这些压力没有显著变化。这些结果表明，缺水动物输尿管梗阻后的血管舒张是由前列腺素释放引起的，可被吲哚美辛消除，而容量扩张动物输尿管梗阻导致的血管舒张可能受其他机制影响。
