Effect of Inhaling 100% O₂ on Ventilation and Acid-Base Balance in Cerebrospinal Fluid of Neonates

Abstract

If 100% O₂ produces hyperventilation by increasing central CO₂ due to cerebral vasoconstriction or diminished reduction of oxyhemoglobin, then, there should be a parallel decrease in alveolar and CSF PCO₂ during O₂ breathing in neonates. To test this hypothesis, we measured ventilation, alveolar PCO₂ and CSF PCO₂, pH and HCO₂ before and 10–20 min after infants began breathing 100% O₂. With 100% O₂, minute ventilation increased from 0.193 ± (SE) 0.013 (n = 7) to 0.252 ± 0.013 liter/min/kg (p < 0.015), P_ACO₂ decreased from 42 ± 2 to 38 ± 2 mm Hg (p < 0.005), CSF PCO₂ decreased from 51 ± 1 to 44 ± 1 mm Hg (p < 0.015), and pH increased from 7.308 ± 0.013 to 7.354 ± 0.013 (p < 0.05). CSF bicarbonate decreased, but not significantly. These findings, showing a trend toward alkalosis, suggest that the neonate, like the adult man, induces hyperventilation during hyperoxia via an increase in PCO₂ at the central level.

Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neurons

“…The "stimulant effect of oxygen which tends to increase respiration" (21) is well documented in human infants (16,56,58) and adults (4,15,21,28,35,36,55,57) and various animal models (27,41,69). Because the dose of hyperoxia, and therefore ROS, is defined by the duration of the hyperoxic exposure and the level of hyperoxia, it is useful to examine studies that have used short and long exposures as well as different levels of hyperoxia at normobaric and hyperbaric pressures.…”

“…Conversely, prolonged exposures to HBO 2 initially stimulates breathing but then leads to respiratory distress and, ultimately, respiratory failure. 5) O 2 -induced hyperventilation significantly reduces PET CO 2 (4,16,35,36,57), which blunts or masks (55) the magnitude of the O 2 -induced hyperventilation. Thus hyperoxic hyperventilation is best measured during isocapnic hyperoxia (4, 55, 57).…”

“…The most frequently cited hypotheses are that hyperoxia 1) decreases cerebral blood flow (CBF) and 2) decreases formation of reduced hemoglobin, thereby interfering with CO 2 transport (the "Haldane effect"). The net effect is to increase PCO 2 in the cerebral vasculature and neural tissue, which stimulates central CO 2 chemoreceptors (16,35,36,55). 3) Lactic acidosis resulting from HBO 2 -induced histotoxic hypoxia within the brain stem may also stimulate central chemoreceptors (14).…”

“…3) Lactic acidosis resulting from HBO 2 -induced histotoxic hypoxia within the brain stem may also stimulate central chemoreceptors (14). These effects of CO 2 and H ϩ are likely to be counterbalanced by the rapidly ensuing respiratory alkalosis that results from O 2 -induced hyperventilation (16). 4) In addition, it was proposed that O 2 disinhibits an inhibitory input that is normally active in normoxia (41).…”

“…The maximum level of inspired PO 2 (PI O 2 ) in our natural environment is only 160 Torr (0.21 O 2 ϫ 760 Torr at sea level ϭ 160 Torr O 2 ϭ 0.21 ATA O 2 ). Regardless, understanding the central effect of hyperoxia on respiratoryrelated neurons (21,44,57,72) becomes very important considering the pervasive use of hyperoxia in respiratory control research (4,13,16,27,71), clinical medicine (3,9,57,64), and civilian and military professions (18).…”