THE EFFECT OF HYPERCAPNIA UPON INTRACELLULAR pH IN THE BRAIN, EVALUATED BY THE BICARBONATE‐ CARBONIC ACID METHOD AND FROM THE CREATINE PHOSPHOKINASE EQUILIBRIUM
Bo K. Siesjö, Jaroslava Folbergrová, V. MacMillan
Abstract
Bo K. Siesjö, Jaroslava Folbergrová, V. MacMillan
Abstract
Abstract— Abstract‐Intracellular pH in the brain was evaluated by the bicarbonate‐carbonic acid method and from the creatine phosphokinase equilibrium, in rats exposed to 6–40 % CO2 for 45 min. There was a very good agreement between the two methods, indicating that the creatine phosphokinase equilibrium in vivo shows the pH dependence predicted from previous in vitro studies. The stepwise increase in the tissue CO2 tension from 45 to 265 mm Hg resulted in a lowering of the intracellular pH from 7.04 to 6.68. The regulation of intracellular pH in hypercapnia was far better than that which can be predicted from physicochemical buffering alone, and calculations indicate that the intracellular buffer base concentration increased by more than 10 mequiv./kg at the maximal Pco2 values encountered.
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Abstract— Abstract‐Intracellular pH in the brain was evaluated by the bicarbonate‐carbonic acid method and from the creatine phosphokinase equilibrium, in rats exposed to 6–40 % CO2 for 45 min. There was a very good agreement between the two methods, indicating that the creatine phosphokinase equilibrium in vivo shows the pH dependence predicted from previous in vitro studies. The stepwise increase in the tissue CO2 tension from 45 to 265 mm Hg resulted in a lowering of the intracellular pH from 7.04 to 6.68. The regulation of intracellular pH in hypercapnia was far better than that which can be predicted from physicochemical buffering alone, and calculations indicate that the intracellular buffer base concentration increased by more than 10 mequiv./kg at the maximal Pco2 values encountered.
Key concepts: Intracellular pH, Carbonic acid, Bicarbonate, Hypercapnia, Intracellular, Chemistry, Creatine kinase, Creatine