Regulation of CSF[HCO3-] during long-term hypoxic hypocapnia in man

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Abstract
During chronic hypoxic hypocapnia compensatory reductions in CSF [HCO3-] were hypothesized to be dependent on a reduced plasma [HCO3-]. In 10 normals, mild metabolic alkalosis was induced by daily NaHCO3 ingestion or K+ depletion by thiazide diuretics. [HCO3-]a was maintained, uninterrupted, at 3-5 meq/1 > control for 5-10 days at 250 m and 1-3 meq/1 > control as ventilation increased and hypocapnia progressed in a near normal fashion over the initial 4-6 days at 3200 m. Some fall in [HCO3-]a could not be prevented during sojourn below those levels achieved in the steady state of metabolic alkalosis immediately prior to ascent. However, the corresponding reductions in CSF [HCO3-] exceeded those in plasma in all sojourners, to the extent that compensation of CSF [H+] after 4-6 days at 3200 m was identical (66%) in subjects with elevated [HCO3-]a and those who acclimatized normally with low [HCO3-]a. Further study of 4 subjects in whom metabolic alkalosis was induced or stopped for 3-4 days, following an initial 4-8 days at 3200 m, confirmed that changes in CSF [HCO3-] during prolonged hypocapnia followed changes in CSF PCO2 [partial pressure CO2], regardless of the level of plasma PCO2 or [HCO3-] or their direction or magnitude of change. While a changing plasma [HCO3-] may contribute in part to the observed regulation of CSF [HCO3-], some mechanism(s) sensitive to, or at least correlated with, brain PCO2 possibly exerts a significant control over CSF [HCO3-] during chronic hypoxic hypocapnia in man. The time course and/or magnitude of ventilatory acclimatization to high altitude were not correlated with changes in CSF [H+] and were not significantly affected by changing CSF-plasma gradients for [HCO3-] or [H+].

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