Ventilatory Acclimatization to Moderate Hypoxemia in Man

Abstract

This study has assessed the regulation of arterial blood andcerebrospinal fluid (CSF) pH and thereby their contribution tothe control of breathing in normal man during various stages ofventilatory acclimatization to 3,100 m altitude. CSF acid-basestatus was determined: (a) from measurements of lumbar spinalfluid during steady-state conditions of chronic normoxia (250 maltitude) and at + 8 h and + 3-4 wk of hypobaric hypoxia; and (b)from changes in cerebral venous P(CO2) at + 1 h hypoxic exposure.After 3-4 wk at 3,100 m, CSF [H(+)] remained significantlyalkaline to values obtained in either chronic normoxia or with 1h hypoxic exposure and was compensated to the same extent (approximately 66%) as was arterial blood [H(+)]. Ventilatoryacclimatization to 3,100 m bore no positive relationship toaccompanying changes in arterial P(O2) and pH and CSF pH: (a) CSFpH either increased or remained constant at 8 h and at 3-4 wkhypoxic exposure, respectively, coincident with significant,progressive reductions in Pa(CO2); (b) arterial P(O2) and pHincreased progressively with time of exposure; and (c) in thesteady-state of acclimatization to 3,100 m the combination ofchemical stimuli present, i.e. Pa(O2) = 60 mm Hg, pHa and pH(CSF)= + 0.03-0.04 > control, was insufficient to produce the observedhyperventilation (Pa(CO2) = 32 mm Hg). It was postulated thatventilatory acclimatization to 3,100 m altitude was mediated byfactors other than CSF [H(+)] and that the combination of chronichypoxemia and hypocapnia of moderate degrees provided nomechanisms for the specific regulation of CSF [H(CO3) (-)] andhence for homeostasis of CSF [H(+)].