Solez K, Ponchak S, Buono R A, Vernon N, Finer P M, Miller M, Heptinstall R H
Am J Physiol. 1976 Nov;231(5 Pt. 1):1315-21. doi: 10.1152/ajplegacy.1976.231.5.1315.
To test the thesis that ureteral obstruction causes medullary ischemia, we determined inner medullary plasma flow (IMPF) in rats with bilateral or unilateral ureteral obstruction, and after relief of obstruction, by the intravenous 125I-albumin infusion technique. A progressive decline in IMPF was observed during obstruction of 18 h duration, greater in bilateral obstruction (7% of normal at 5h) than in unilateral obstruction (28% of normal at 5 h). The elevation in ureteral pressure was greater and more sustained in bilateral obstruction. After relief of obstruction, IMPF rose to 69-78% of normal in both groups within 2 h. Histologic studies showed tubular necrosis in portions of the inner and outer medulla immediately beneath the renal pelvic epithelium after bilateral or unilateral obstruction of 18 h duration, and India ink perfusion studies showed very poor filling of vasa recta in these areas. The concentrating defect in the postobstructive kidney may be related, at least in part, to damage inflicted by medullary ischemia during obstruction.
为了验证输尿管梗阻会导致髓质缺血这一论点,我们采用静脉注射125I-白蛋白灌注技术,测定了双侧或单侧输尿管梗阻大鼠以及梗阻解除后的肾内髓质血浆流量(IMPF)。在持续18小时的梗阻过程中,观察到IMPF逐渐下降,双侧梗阻(5小时时为正常的7%)比单侧梗阻(5小时时为正常的28%)下降幅度更大。双侧梗阻时输尿管压力升高幅度更大且持续时间更长。梗阻解除后,两组的IMPF在2小时内均升至正常的69%-78%。组织学研究显示,在持续18小时的双侧或单侧梗阻后,肾盂上皮下方的内髓质和外髓质部分出现肾小管坏死,印度墨汁灌注研究显示这些区域的直小血管充盈极差。梗阻后肾脏的浓缩功能缺陷可能至少部分与梗阻期间髓质缺血造成的损伤有关。