Conger J D
Circ Shock. 1983;11(3):235-44.
Male Sprague-Dawley rats were used to investigate renal vascular abnormalities in the maintenance phase of norepinephrine-induced ischemic acute renal failure. In this model uremia peaks in the first 5 days with progressive recovery of renal function which approaches control at 25 days. Renal blood flow returns to normal in the first week. Micropuncture experiments revealed that there was a dual nephron population during the first 3 days of acute renal failure. The majority of proximal tubules had elevated pressures from tubular obstruction. The nephron filtration rate responses in these nephrons were similar to normal if tubular obstruction was relieved, indicating that glomerular filtration dynamics were not impaired. In other nephrons tubular pressures were low, and venting the tubules did not increase nephron filtration. In these nephrons glomerular blood flowed and capillary pressures were reduced. There was no evidence of tubular fluid backleak from 14C-inulin microperfusion. A second vascular abnormality was an absence of renal blood flow autoregulation at 1 week in acute renal failure. The autoregulatory defect could be corrected by renal denervation.
采用雄性Sprague-Dawley大鼠研究去甲肾上腺素诱导的缺血性急性肾衰竭维持期的肾血管异常。在该模型中,尿毒症在最初5天达到高峰,随后肾功能逐渐恢复,在25天时接近正常水平。肾血流量在第一周恢复正常。微穿刺实验显示,在急性肾衰竭的前3天存在两种不同的肾单位群体。大多数近端小管因肾小管阻塞而压力升高。如果肾小管阻塞得到缓解,这些肾单位的肾单位滤过率反应与正常情况相似,这表明肾小球滤过动力学未受损。在其他肾单位中,肾小管压力较低,对肾小管进行引流并不会增加肾单位滤过。在这些肾单位中,肾小球血流和毛细血管压力降低。14C-菊粉微灌注实验未发现肾小管液反流的证据。第二个血管异常是急性肾衰竭1周时肾血流量自动调节功能缺失。这种自动调节缺陷可通过肾去神经支配来纠正。