Role of Cerebrospinal Fluid [H+] in Ventilatory Deacclimatization from Chronic Hypoxia

Abstract

A C T Once ventilatory acclinmatizationi begins in sea level residents sojourning at high altitude, abrupt restoration of normal oxygen tensions will not restore ventilation to normal. We have investigated the role of cerebrospinal fluid (CSF) [He] in this sustained hyperventilation by measurinig CSF acid-base status in seven imien (lumbar) and five ponies (cisterinal) in normoxia, first at sea level anid then periodically over 13-24 h of"deacclimatization" after 3-5 d in hypoxia (PB = 440 mm Hg). After 1 h deaccliimcatization, hyperventilation continued at a level only slightly less than that obtained in chronic hypoxia (+ 1-2 mm Hg PA,O2), whereas CSF pH was either e(lual (in man) or alkaline (in pony, +0.02, P < 0.01) to sea level values. Between 1 and 12-13 h deacclimatization in all humans and ponies VA fell progressively (PA(,0( increased 4-7 mm Hg) and CSF pH became increasingly more acid (-0.02 to -0.05, P < 0.01). Between 12 acnd 24 h of normoxic deacclimatization in ponies, PAco, rose further toward norinal, coincideint with an increasing acidity in CSF (-0.02 pH). Similar negative correlations were found between changes in arterial pH and VA throughout normoxic deaccliimiatization. We conclude that [H+] in the lumbar or cisternal CSF is not the mediator of the continued hyperventilation and its gradual dissipation with time during normoxic deacclimatization from chronic hypoxia. These negative relationships of VA to CSF [H+] in normoxia are analogous to those previously shown during acclimatization to hypoxia.