Blantz R C
J Clin Invest. 1974 Nov;54(5):1135-43. doi: 10.1172/JCI107857.
The effect of mannitol upon glomerular ultrafiltration was examined in hydropenic Munich-Wistar rats. Superficial nephron filtration rate (sngfr) rose from 32.0+/-0.9 nl/min/g kidney wt to 42.0+/-1.6 (P < 0.001) in eight rats. Hydrostatic pressure gradients acting across the glomerular capillary (DeltaP) were measured in glomerular capillaries and Bowman's space with a servo-nulling device, systemic (piA) and efferent arteriolar oncotic pressures (piE) were determined by microprotein analysis. These data were applied to a computer-based mathematical model of glomerular ultrafiltration to determine the profile of effective filtration pressure (EFP = DeltaP - pi) and total glomerular permeability (L(p)A) in both states. Filtration equilibrium obtained in hydropenia (L(p)A >/= 0.099+/-0.006 nl/s/g kidney wt/mm Hg) and sngfr rose because EFP increased from a maximum value of 4.2+/-1.1 to 12.8+/-0.5 mm Hg after mannitol (P <0.01). This increase was due to both increased nephron plasma flow and decreased piA. Computer analysis of these data revealed that more than half (>58%) of this increase was due to decreased piA, consequent to dilution of protein. Since EFP was disequilibrated after mannitol, L(p)A could be calculated accurately (0.065 +/- 0.003 nl/s/g kidney wt/mm Hg) and was significantly lower than the minimum estimate in hydropenia.Therefore, sngfr does increase with mannitol and this increase is not wholly dependent upon an increase in nephron plasma flow since the major factor increasing EFP was decreased piA.
在缺水的慕尼黑-维斯塔大鼠中研究了甘露醇对肾小球超滤的影响。8只大鼠的浅表肾单位滤过率(sngfr)从32.0±0.9 nl/分钟/克肾重升至42.0±1.6(P<0.001)。用伺服归零装置测量肾小球毛细血管和鲍曼氏间隙之间的跨肾小球毛细血管静水压梯度(ΔP),通过微量蛋白分析确定全身(πA)和出球小动脉胶体渗透压(πE)。将这些数据应用于基于计算机的肾小球超滤数学模型,以确定两种状态下有效滤过压(EFP = ΔP - π)和总肾小球通透性(L(p)A)的情况。缺水时达到滤过平衡(L(p)A≥0.099±0.006 nl/秒/克肾重/毫米汞柱),sngfr升高是因为甘露醇后EFP从最大值4.2±1.1升至12.8±0.5毫米汞柱(P<0.01)。这种升高是由于肾单位血浆流量增加和πA降低。对这些数据的计算机分析表明,这种升高的一半以上(>58%)是由于蛋白质稀释导致πA降低。由于甘露醇后EFP失衡,可以准确计算L(p)A(0.065±0.003 nl/秒/克肾重/毫米汞柱),且显著低于缺水时的最低估计值。因此,sngfr确实会因甘露醇而增加,且这种增加并非完全依赖于肾单位血浆流量的增加,因为增加EFP的主要因素是πA降低。