Clark D D, Chang B S, Garella S G, Cohen J J, Madias N E
Kidney Int. 1983 Feb;23(2):336-41. doi: 10.1038/ki.1983.24.
Studies have demonstrated that the protective effect of secondary hypocapnia on plasma acidity during chronic HCl-acidosis is undermined by a renal-mediated decrement in plasma bicarbonate concentration induced by the hypocapnia itself. The present study was designed to assess whether the protection of "whole body" intracellular pH (pHi) is similarly undermined by this maladaptive response of the kidney. Whole body pHi was estimated by the 5,5 dimethyl-2,4-oxazolidinedione (DMO) method in seven unanesthetized dogs under each of three conditions: control, chronic HCl-acidosis (10 mEq H+/kg/day) with spontaneous secondary hypocapnia, and chronic HCl-acidosis with a normal level of carbon dioxide tension (maintained by the use of an environmental chamber). pHi was 6.71 +/- 0.02 during control, and 6.57 +/- 0.03 and 6.57 +/- 0.02 during the two acidosis periods, respectively. These results indicate that sustained secondary hypocapnia fails to render the intracellular compartment less acidic because of a maladaptive reduction in intracellular bicarbonate concentration.
研究表明,在慢性盐酸酸中毒期间,继发性低碳酸血症对血浆酸度的保护作用会被低碳酸血症本身引起的肾脏介导的血浆碳酸氢盐浓度降低所削弱。本研究旨在评估肾脏的这种适应性不良反应是否同样会削弱对“全身”细胞内pH值(pHi)的保护作用。通过5,5-二甲基-2,4-恶唑烷二酮(DMO)方法,在三种条件下对七只未麻醉的狗的全身pHi进行了估计:对照、伴有自发性继发性低碳酸血症的慢性盐酸酸中毒(10 mEq H⁺/kg/天),以及二氧化碳张力正常的慢性盐酸酸中毒(通过使用环境舱维持)。对照期间pHi为6.71±0.02,在两个酸中毒期间分别为6.57±0.03和6.