Rose C E, Anderson R J, Carey R M
Am J Physiol. 1984 Jul;247(1 Pt 2):R127-34. doi: 10.1152/ajpregu.1984.247.1.R127.
To determine the effects of acute blood gas derangements on renal water and solute excretion and vasopressin secretion, six unanesthetized mongrel dogs were studied during 1) combined acute hypoxemia and hypercapnic acidosis [arterial O2 partial pressure (PaO2) 36 +/- 1 Torr, arterial CO2 partial pressure (PaCO2) 54 +/- 2 Torr, pH 7.18 +/- 0.01], 2) acute hypoxemia (PaO2 33 +/- 2 Torr, PaCO2 33 +/- 1 Torr, pH 7.34 +/- 0.01), and 3) acute hypercapnic acidosis (PaO2 83 +/- 3 Torr, PaCO2 53 +/- 1 Torr, pH 7.19 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis increased (P less than 0.05) mean arterial pressure, but renal hemodynamic function deteriorated with decreased (P less than 0.05) glomerular filtration rate and increased (P less than 0.05) renal vascular resistance. Moreover free water clearance became more negative (P less than 0.05) and urine osmolality increased (P less than 0.05). During acute hypoxemia or acute hypercapnic acidosis alone, mean arterial pressure and renal hemodynamic function were unchanged but free water clearance became more negative (P less than 0.05). During acute hypoxemia, urine osmolality increased (P less than 0.05) comparably with values observed during combined acute hypoxemia and hypercapnic acidosis. Plasma vasopressin concentrations increased profoundly (P less than 0.05) during combined hypoxemia and hypercapnic acidosis and during acute hypoxemia alone and were significantly elevated (P less than 0.05) above the increased plasma vasopressin concentrations observed during acute hypercapnic acidosis. We conclude that acute hypoxemia and hypercapnic acidosis result in impairment of renal water excretion, probably mediated through vasopressin secretion.
为了确定急性血气紊乱对肾脏水和溶质排泄以及血管加压素分泌的影响，对6只未麻醉的杂种狗进行了研究，研究期间分别处于以下三种状态：1）急性低氧血症合并高碳酸性酸中毒[动脉血氧分压（PaO2）36±1托，动脉血二氧化碳分压（PaCO2）54±2托，pH值7.18±0.01]；2）急性低氧血症（PaO2 33±2托，PaCO2 33±1托，pH值7.34±0.01）；3）急性高碳酸性酸中毒（PaO2 83±3托，PaCO2 53±1托，pH值7.19±0.02）。急性低氧血症合并高碳酸性酸中毒使平均动脉压升高（P<0.05），但肾脏血液动力学功能恶化，肾小球滤过率降低（P<0.05），肾血管阻力增加（P<0.05）。此外，自由水清除率变得更负（P<0.05），尿渗透压升高（P<0.05）。单独处于急性低氧血症或急性高碳酸性酸中毒期间，平均动脉压和肾脏血液动力学功能未改变，但自由水清除率变得更负（P<0.05）。在急性低氧血症期间，尿渗透压升高（P<0.05），与急性低氧血症合并高碳酸性酸中毒期间观察到的值相当。在低氧血症合并高碳酸性酸中毒期间以及单独的急性低氧血症期间，血浆血管加压素浓度显著升高（P<0.05），且明显高于急性高碳酸性酸中毒期间观察到的升高的血浆血管加压素浓度（P<0.05）。我们得出结论，急性低氧血症和高碳酸性酸中毒导致肾脏水排泄受损，可能是通过血管加压素分泌介导的。
