Bird J E, Evan A P, Peterson O W, Blantz R C
Department of Medicine, University of California, San Diego School of Medicine.
Kidney Int. 1989 Jun;35(6):1282-9. doi: 10.1038/ki.1989.123.
Renal ischemia followed by two hours of reperfusion produces a complex form of acute renal failure characterized by a reduction in nephron filtration rate (SNGFR) and moderate proximal tubular damage. We have examined glomerular hemodynamics, SNGFR and histologic changes after renal ischemia and two hours of reperfusion in untreated (I) rats and rats pretreated with the antioxidant, probucol (IP). SNGFR decreased significantly by 47% in I rats. Reduction in SNGFR was primarily the result of a major decrease in the glomerular capillary hydrostatic pressure gradient, delta P, and a decrease in nephron plasma flow (SNPF). The glomerular ultrafiltration coefficient remained equal to control valves. In IP rats SNGFR was improved to values 89% of control rats due to higher values of delta P and SNPF. Histologic evidence of modest damage to cells of the proximal tubule was equal in both untreated and probucol treated ischemic animals. These studies demonstrate that: (a) primary reductions in nephron filtration rate at the glomerulus result from decreases in delta P and nephron plasma flow; b) pretreatment with the antioxidant, probucol, increases nephron plasma flow and SNGFR, and maintains more normal values for delta P; and c) tubular damage was equivalent in I and IP rats in spite of differences in SNGFR.
肾脏缺血两小时后再灌注会引发一种复杂形式的急性肾衰竭，其特征为肾单位滤过率（单个肾单位肾小球滤过率，SNGFR）降低以及中度近端肾小管损伤。我们研究了未处理的（I）大鼠和用抗氧化剂普罗布考预处理的大鼠（IP）在肾脏缺血及两小时再灌注后的肾小球血流动力学、SNGFR及组织学变化。I组大鼠的SNGFR显著降低了47%。SNGFR降低主要是由于肾小球毛细血管静水压梯度（ΔP）大幅下降以及肾单位血浆流量（SNPF）减少所致。肾小球超滤系数仍与对照值相等。在IP组大鼠中，由于ΔP和SNPF值较高，SNGFR改善至对照大鼠值的89%。未处理和普罗布考处理的缺血动物近端小管细胞轻度损伤的组织学证据相同。这些研究表明：（a）肾小球处肾单位滤过率的原发性降低是由ΔP和肾单位血浆流量减少引起的；（b）用抗氧化剂普罗布考预处理可增加肾单位血浆流量和SNGFR，并使ΔP维持在更正常的值；（c）尽管SNGFR存在差异，但I组和IP组大鼠的肾小管损伤程度相同。
