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Anesthetized, paralyzed dogs after a control period at normal pHa were hyperventilated to produce a hypocapnic alkalosis. The pH, PCO2, (HCO3 minus), and (lactate) in cisternal and lumbar CSF and arterial blood were determined at normal conditions (control) shortly after induction of respiratory alkalosis (time 0) and 3, 4.5, and 6 h thereafter. These values along with measurements of the CSF/plasma DC potential (E) allowed calculations of the electrochemical potential difference (mu) between CSF and blood for H+ and HCO3 minus. After 6 h of hypocapnic alkalosis, muH+ and muHCO3 minus had returned to minus 0.7 and minus 1.0 mV of control at the cistern and to minus 1.0 and +0.4 mV of control for lumbar CSF. This return of mu is compatible with a passive distribution of these ions though active ion regulation is not ruled out. Assuming passive distribution, differences in deltaE/DELTApHa between metabolic and respiratory acid-base changes determined the extent of CSF pH homeostasis during compensated acid-base derangements.
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