Effects of moderate hypoxemia and hypocapnia on CSF [H+] and ventilation in man.
The effects of 26 h of normoxic hypocapnia (PaCO2, 31 MMHg) vs. 26 h of hypocapnia plus hypobaric hypoxia (PaCO2 32, PaO2 57 mmHg) were compared with respect to: a) CSF acid-base status; and b) the spontaneous ventilation (at PIO2 145 mmHg) which followed the imposed (voluntary) hyperventilation. For each condition of prolonged hypocapnia, PaCO2 was held constant throughout and pHa and [HCO3-]a were constant over the final 6-10 h. We assumed that measured changes in lumbar CSF acid-base status paralleled those in cisternal CSF. Spontaneous hyperventilation followed both normoxic and hypoxic hypocapnia but was significantly greater following hypoxic hypocapnia. In the CSF, pH compensation after 26 h of hyperventilation was incomplete (similar to 45-50%), was similar to that in arterial blood, and was unaffected by a superimposed hypoxemia. These data were inconsistent with current theory which proposes the regulation of CSF [HCO2] via local mechanisms and, in turn, the mediation of ventilatory acclimatization to hypoxemia and/or hypocapnia via CSF [H+]. Alternative mediators of ventilatory acclimatization were postulated, including mechanisms both dependent on and independent of "chemoreceptor" stimuli.
D000136:Acid-Base Equilibrium; D000328:Adult; D001639:Bicarbonates / Q000097:blood / Q000134:cerebrospinal fluid; D001827:Body Height; D001835:Body Weight; D002245:Carbon Dioxide / Q000097:blood*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000097:blood / Q000134:cerebrospinal fluid*; D008297:Male; D012119:Respiration; D013147:Spirometry; D013997:Time Factors
D001639:Bicarbonates; D002245:Carbon Dioxide