Ott C E, Haas J A, Cuche J L, Knox F G
J Clin Invest. 1975 Mar;55(3):612-20. doi: 10.1172/JCI107969.
The effect of increased peritubule capillary oncotic pressure on sodium reabsorption by the proximal tubule of the dog was investistigated after extracellular volume expansion (ECVE) with Ringer's solution or during continued hydropenia. Control measurements were made after ECVE or during hydropenia and again during renal arterial infusion with hyperoncotic albumin solution. Absolute reabsorption by the proximal tubule was calculated from fractional reabsorption and single nephron filtration rates as determined by micropuncture. Direct measurements of efferent arteriole protein were used to determine efferent arteriolar oncotic pressure. Albumin infused into the renal artery after ECVE significantly increased efferent oncotic pressure by 17.6 plus or minus 5.3 mm Hg. Fractional and absolute reabsorption by the proximal tubule increased from 20 plus or minus 6 to 37 plus or minus 5% and from 22 plus or minus 6 to 36 plus or minus 7 nl/min, respectively. During hydropenia, the albumin infusion significantly increased efferent oncotic pressure by 15.0 plus or minus 4.4 mm Hg. However, in contrast to the effect seen during ECVE, neither fractional nor absolute reabsorption was changed, delta equals 0.3 plus or minus 1.5% and 3 plus or minus 5 nl/min, respectively. Single nephron filtration rates were not significantly different between the groups and were unchanged by the albumin infusion. Peritubule capillary hydrostatic pressures, measured with a null-servo device, were not changed by the albumin infusion in either group. Renal interstitial hydrostatic pressure, measured from chronically implanted polyethylene capsules, was decreased significantly from 7.2 plus or minus 0.9 to 3.4 plus or minus 0.6 mm Hg in the hydropenic group and from 0.6 plus or minus 0.6 to 4.8 plus or minus 0.7 mm Hg in the Ringer's expanded group. In the hydropenic group, the increase in efferent oncotic pressure was nearly compensated for by changes in interstitial forces so that the calculated net force for capillary uptake was almost unchanged, 17.8 mm Hg before vs. 21.4 mm Hg during the albumin infusion. The increased efferent oncotic pressure in the Ringer's expanded group was not compensated, so that the calculated net force for uptake was increased, 11.9 mm Hg before to 22.2 mm Hg during the albumin infusion. Thus, while the increase in efferent oncotic pressure during albumin infusion was not significantly different between the groups, absolute and fractional reabsorptions were increased only in the animals in which the extracellular volume was expanded. The results suggest that ECVE alters the effect of increased peritubule oncotic pressure on sodium reabsorption by the proximal tubule.
在用林格氏液进行细胞外液量扩张(ECVE)后或在持续缺水期间,研究了肾小管周围毛细血管胶体渗透压升高对犬近端小管钠重吸收的影响。在ECVE后或缺水期间以及在肾动脉输注高渗白蛋白溶液期间进行对照测量。近端小管的绝对重吸收是根据微量穿刺测定的重吸收分数和单肾单位滤过率计算得出的。通过直接测量出球小动脉蛋白来确定出球小动脉胶体渗透压。ECVE后注入肾动脉的白蛋白使出球胶体渗透压显著升高17.6±5.3mmHg。近端小管的重吸收分数和绝对重吸收分别从20±6%增加到37±5%,以及从22±6nl/min增加到36±7nl/min。在缺水期间,白蛋白输注使出球胶体渗透压显著升高15.0±4.4mmHg。然而,与ECVE期间的效应相反,重吸收分数和绝对重吸收均未改变,分别为δ=0.3±1.5%和3±5nl/min。各实验组之间的单肾单位滤过率无显著差异,且白蛋白输注后未发生变化。用零伺服装置测量的肾小管周围毛细血管静水压在两组中均未因白蛋白输注而改变。通过长期植入的聚乙烯胶囊测量的肾间质静水压在缺水组中从7.2±0.9mmHg显著降低至3.4±0.6mmHg,在林格氏液扩张组中从0.6±0.6mmHg降低至4.8±0.7mmHg。在缺水组中,出球胶体渗透压的升高几乎被间质力的变化所抵消,因此计算得出的毛细血管摄取净力几乎未变,白蛋白输注前为17.8mmHg,输注期间为21.4mmHg。林格氏液扩张组中出球胶体渗透压的升高未得到补偿,因此计算得出的摄取净力增加,白蛋白输注前为11.9mmHg,输注期间为22.2mmHg。因此,虽然白蛋白输注期间出球胶体渗透压的升高在两组之间无显著差异,但绝对和分数重吸收仅在细胞外液量扩张的动物中增加。结果表明,ECVE改变了肾小管周围胶体渗透压升高对近端小管钠重吸收的影响。