Arieff A I, Kerian A, Massry S G, DeLima J
Am J Physiol. 1976 Mar;230(3):804-12. doi: 10.1152/ajplegacy.1976.230.3.804.
To evaluate the metabolic adaptations of the brain to acute respiratory acid-base disturbances, a method was developed to measure intracellular pH (pHi) in the brain of dogs under conditions in which arterial pH is rapidly altered. Brain pHi was determined by measuring the distribution of 14C-labeled dimethadione (DMO) in brain relative to cortical CSF. Brain extracellular space (ECS) was evaluated as the 35SO4 = space relative to cortical CSF, and arterial Po2 was maintained at 82-110 mmHg. In normal dogs, brain (cerebral cortex) pHi was 7.05, and after 1 h of hypercapnia (arterial pH = 7.07) it fell to 6.93. However, after 3 h with arterial Pco2 maintained at 85 mmHg brain pHi was normal (7.06), and during this time brain bicarbonate had risen from 11.3 to 24.4 meq/kg H2O. These changes were not prevented by intravenous doses of acetazolamide,
为评估大脑对急性呼吸性酸碱紊乱的代谢适应性，开发了一种方法来测量犬脑在动脉pH快速改变条件下的细胞内pH（pHi）。通过测量相对于皮质脑脊液的14C标记二甲双酮（DMO）在脑中的分布来确定脑pHi。将脑细胞外间隙（ECS）评估为相对于皮质脑脊液的35SO4=间隙，并将动脉血氧分压维持在82-110 mmHg。在正常犬中，脑（大脑皮质）pHi为7.05，高碳酸血症1小时后（动脉pH=7.07）降至6.93。然而，在动脉二氧化碳分压维持在85 mmHg 3小时后，脑pHi恢复正常（7.06），在此期间脑碳酸氢盐从11.3 meq/kg H2O升至24.4 meq/kg H2O。静脉注射乙酰唑胺未能阻止这些变化。
