Respiratory control at high altitude suggesting active transport regulation of CSF pH

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Abstract
The role of CSF pH and HCO–3 ion in stimulating respiration was studied in four men during acclimatization from sea level to 3,800 m for 8 days. Mean values for sea level control, 2nd day and 8th day at altitude were, for CSF 7.328, 7.338, and 7.336, and for arterial blood 7.424, 7.485, and 7.484. Ventilatory response to four levels of alveolar CO2 was determined while subjects breathed high oxygen to eliminate peripheral chemoreceptor drive, and for each value of PaCOCO2, arterial and CSF pH were computed. The displacement of the ventilation response curves at altitude from the sea level curves was: -10 mm Hg PaCOCO2, + 0.06 pH unit for arterial blood, but -0.01 for CSF pH. CSF HCO3 was 4–5 mEq/liter lower than control within 1–2 days at altitude, whereas renal buffer base excretion only reduced blood standard bicarbonate 1 mEq/liter after a week. CSF chloride and lactate rose about 6 and 1 mEq/liter. Thus, medullary respiratory chemoreceptor drive, initially reduced at altitude by hyperventilation alkalosis, is restored to normal during acclimatization by reduction in CSF HCO3, the incremental ventilatory drive being supplied by peripheral chemoreceptors. The blood-CSF barrier appears to respond to the initial hyperventilation alkalosis by actively reducing CSF HCO3; the data suggest that CSF pH is thus regulated by active transport by the blood-CSF barrier. altitude acclimatization; blood brain barrier; regulation of respiration Submitted on December 17, 1962

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