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Free access | 10.1172/JCI107646

Ventilatory Acclimatization to Moderate Hypoxemia in Man: THE ROLE OF SPINAL FLUID [H+]

J. A. Dempsey, H. V. Forster, and G. A. Dopico

Pulmonary Physiology Laboratory, Department of Preventive Medicine, University of Wisconsin Medical School, Madison, Wisconsin 53706

Find articles by Dempsey, J. in: PubMed | Google Scholar

Pulmonary Physiology Laboratory, Department of Preventive Medicine, University of Wisconsin Medical School, Madison, Wisconsin 53706

Find articles by Forster, H. in: PubMed | Google Scholar

Pulmonary Physiology Laboratory, Department of Preventive Medicine, University of Wisconsin Medical School, Madison, Wisconsin 53706

Find articles by Dopico, G. in: PubMed | Google Scholar

Published April 1, 1974 - More info

Published in Volume 53, Issue 4 on April 1, 1974
J Clin Invest. 1974;53(4):1091–1100. https://doi.org/10.1172/JCI107646.
© 1974 The American Society for Clinical Investigation
Published April 1, 1974 - Version history
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Abstract

This study has assessed the regulation of arterial blood and cerebrospinal fluid (CSF) pH and thereby their contribution to the control of breathing in normal man during various stages of ventilatory acclimatization to 3,100 m altitude. CSF acid-base status was determined: (a) from measurements of lumbar spinal fluid during steady-state conditions of chronic normoxia (250 m altitude) and at + 8 h and + 3-4 wk of hypobaric hypoxia; and (b) from changes in cerebral venous PCO2 at + 1 h hypoxic exposure. After 3-4 wk at 3,100 m, CSF [H+] remained significantly alkaline to values obtained in either chronic normoxia or with 1 h hypoxic exposure and was compensated to the same extent (∼66%) as was arterial blood [H+]. Ventilatory acclimatization to 3,100 m bore no positive relationship to accompanying changes in arterial PO2 and pH and CSF pH: (a) CSF pH either increased or remained constant at 8 h and at 3-4 wk hypoxic exposure, respectively, coincident with significant, progressive reductions in PaCO2; (b) arterial PO2 and pH increased progressively with time of exposure; and (c) in the steady-state of acclimatization to 3,100 m the combination of chemical stimuli present, i.e. PaO2 = 60 mm Hg, pHa and pHCSF = + 0.03-0.04 > control, was insufficient to produce the observed hyperventilation (PaCO2 = 32 mm Hg). It was postulated that ventilatory acclimatization to 3,100 m altitude was mediated by factors other than CSF [H+] and that the combination of chronic hypoxemia and hypocapnia of moderate degrees provided no mechanisms for the specific regulation of CSF [HCO3−] and hence for homeostasis of CSF [H+].

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