CSF pH and ventilatory acclimatization to altitude

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Abstract
Men (4) at sea level and, after 3 days'' acclimatization at 3810 m altitude, were studied to determine whether hypoxic peripheral chemoreceptor drive is responsible for maintaining the observed alkalosis in CSF at altitude and presumably in medullary respiratory chemoreceptors. Measured were sensitivities to CO2 and hypoxia, lumbar CSF pH during acute normoxia at altitude and the effect of hypoxia at constant PCO2 [CO2 partial pressure] on lumbar CSF PCO2 and pH, presumably acting via local vasodilation. The ventilatory sensitivities to CO2 and hypoxia were unaltered at altitude, except for displacement of all curves to 10 Torr lower PCO2 values. At altitude, acute normoxia (to PaO2 [alveolar O2 partial pressure] = 100 Torr) raised PACO2 3.7 Torr within 5 min, where it remained during a 45 min CSF equilibration period. CSF pH was then 7.307 .+-. 0.016, not significantly different from the sea-level value of 7.312 .+-. 0.027. At both altitudes, isocapnic hypoxia reduced CSF PCO2 1.8 .+-. 1.2 Torr and raised CSF pH 0.021 .+-. 0.007, suggesting a 32% increase in blood flow of cord and other tissue near CSF. At altitude, about 0.007 of the CSF alkalosis can be attributed to cord vasodilation, when the effects of PCO2 on cord blood flow and of hypoxia are considered on central chemoreceptor blood flow. About 0.04 alkaline shift can be directly attributed to the ventilatory drive arising in peripheral chemoreceptors. Without this alkaline central inhibition, peripheral drive would induce a far greater increase in ventilation and PCO2 would fall to about half the observed value. In steady states of respiratory acidosis and alkalosis, CSF pH is not perfectly regulated, its steady-state value reflecting the strength of peripheral chemoreceptor and other ventilatory drives.

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