Gill J R, Casper A G
J Clin Invest. 1969 May;48(5):915-22. doi: 10.1172/JCI106050.
In 12 studies, a femoral artery and vein of a donor dog treated with desoxycorticosterone were connected by tubing to a renal artery and vein of a recipient dog treated with desoxycorticosterone, and the kidney with its nerve supply intact was perfused at femoral arterial pressure. Infusion of normal saline, which contained albumin, from 2.7 to 3.1 g/100 ml, in the donor produced significant natriuresis in a kidney of the donor (from 112 to 532 muEq/min) and in the perfused kidney (from 60 to 301 muEq/min) of the recipient. Increased sodium excretion in the perfused kidney was associated with an increase in the clearances of inulin and para-aminohippurate (P < 0.01) and a decrease in hematocrit of perfusing blood (P < 0.01). Infusion was continued in the donor while recipient was bled 23 ml/kg, with a decrease in mean arterial pressure from 152 to 130 mm Hg. Sodium excretion in perfused kidney decreased from 301 to 142 muEq/min (P < 0.01), whereas sodium excretion in donor was unchanged (506 VS. 532 muEq/min; P > 0.3). Clearance of inulin by perfused kidney was not significantly affected by bleeding (26 +/-SE 2 VS. 25 +/-SE 2; P > 0.2), but the clearance of para-aminohippurate was decreased by bleeding (P < 0.01), so that filtration fraction increased. As the perfused kidney of the recipient dog continued to receive blood from the natriuretic donor dog when the recipient dog was bled, the decrease in sodium excretion that bleeding produced in the perfused kidney was presumably mediated by renal nerves. Thus, an increase in nervous stimuli to the kidney that is not sufficient to decrease glomerular filtration rate can increase the tubular reabsorption of sodium and thereby significantly decrease its excretion. This property of the sympathetic nervous system to affect tubular reabsorption of sodium suggests that an increase in sympathetic activity may constitute an important mechanism for the renal conservation of sodium when intravascular volume is contracted by hemorrhage or other cause.
在12项研究中,将用脱氧皮质酮处理的供体犬的股动脉和静脉通过管道与用脱氧皮质酮处理的受体犬的肾动脉和静脉相连,并且在股动脉压力下对神经供应完整的肾脏进行灌注。向供体输注含白蛋白量为2.7至3.1g/100ml的生理盐水,可使供体的一侧肾脏(从112增至532μEq/分钟)以及受体被灌注肾脏(从60增至301μEq/分钟)出现显著的利钠作用。被灌注肾脏中钠排泄增加与菊粉和对氨基马尿酸清除率升高(P<0.01)以及灌注血液的血细胞比容降低(P<0.01)相关。在受体放血23ml/kg(平均动脉压从152降至130mmHg)时,继续向供体输注生理盐水。被灌注肾脏的钠排泄从301降至142μEq/分钟(P<0.01),而供体的钠排泄未改变(506对532μEq/分钟;P>0.3)。放血对被灌注肾脏菊粉清除率无显著影响(26±标准误2对25±标准误2;P>0.2),但对氨基马尿酸清除率因放血而降低(P<0.01),从而滤过分数增加。当受体犬放血时,其被灌注肾脏继续接受来自利钠供体犬的血液,放血导致被灌注肾脏钠排泄减少大概是由肾神经介导的。因此,对肾脏的神经刺激增加,在不足以降低肾小球滤过率时,可增加肾小管对钠的重吸收,从而显著减少钠的排泄。交感神经系统的这一影响肾小管钠重吸收的特性表明,当血管内容量因出血或其他原因而减少时,交感神经活动增加可能是肾脏保钠的重要机制。