Hellberg P O, Källskog O, Wolgast M
Department of Physiology and Medical Biophysics, University of Uppsala, Biomedical Center, Sweden.
Kidney Int. 1990 Sep;38(3):432-9. doi: 10.1038/ki.1990.223.
Trapping of red blood cells (RBCs) in renal medulla vasculature in postischemic acute renal failure (ARF) was found to depend upon the length of the ischemic period. Thus trapping occurred after 45 minutes but not 25 minutes of ischemia. By prior hemodilution to a hematocrit (hct) of 30%, RBC trapping after 45 minutes of ischemia could be completely prevented. Likewise hemo-concentration (hct = 60%) before 25 minutes of ischemia resulted in extensive RBC trapping. By increasing or decreasing the hct, the contribution of RBC trapping to the functional defects and decrease in renal blood flow that follows minor (25 min) and more substantial (45 min) ischemia was investigated. Renal blood flow (RBF) was measured by microspheres, and vascular and tubular pressure by the micropuncture technique. Glomerular filtration rate (GFR) was estimated from inulin clearance, and tubular function from urine osmolality and sodium and potassium excretion. It was found that postischemic RBF was not correlated to RBC trapping but depended on the length of ischemia. After both 25 and 45 minutes of ischemia tubular obstructions occurred in the proximal tubules and/or loops of Henle, causing an increase in proximal tubular pressure. These obstructions were dependent on the length of ischemia but not on RBC trapping. After hemoconcentration and 25 minutes of ischemia there was an increment in distal tubular pressure, indicating that abundant RBC trapping may contribute to an increase in tubular pressure by compression of medullary tubules and thereby reduce GFR. When the damage was more severe other factors came into play and the contribution of RBC trapping to the decrease in GFR was minimal.(ABSTRACT TRUNCATED AT 250 WORDS)
研究发现，缺血后急性肾衰竭（ARF）时肾髓质血管中红细胞（RBC）的滞留取决于缺血时间的长短。因此，缺血45分钟后会发生红细胞滞留，而25分钟则不会。通过预先将血细胞比容（hct）稀释至30%，可完全防止缺血45分钟后的红细胞滞留。同样，在缺血25分钟前进行血液浓缩（hct = 60%）会导致大量红细胞滞留。通过增加或降低血细胞比容，研究了红细胞滞留对轻度（25分钟）和更严重（45分钟）缺血后功能缺陷及肾血流量减少的影响。用微球测量肾血流量（RBF），用微穿刺技术测量血管和肾小管压力。通过菊粉清除率估算肾小球滤过率（GFR），通过尿渗透压、钠和钾排泄评估肾小管功能。结果发现，缺血后肾血流量与红细胞滞留无关，而是取决于缺血时间的长短。缺血25分钟和45分钟后，近端小管和/或亨利袢均出现肾小管阻塞，导致近端小管压力升高。这些阻塞取决于缺血时间的长短，而与红细胞滞留无关。血液浓缩和缺血25分钟后，远端小管压力升高，表明大量红细胞滞留可能通过压迫髓质小管导致小管压力升高，从而降低肾小球滤过率。当损伤更严重时，其他因素起作用，红细胞滞留对肾小球滤过率降低的影响最小。（摘要截短于250字）
