In:
Neonatology, S. Karger AG, Vol. 38, No. 1-2 ( 1980), p. 85-89
Kurzfassung:
If 100% O 〈 sub 〉 2 〈 /sub 〉 produces hyperventilation by increasing central CO 〈 sub 〉 2 〈 /sub 〉 due to cerebral vasoconstriction or diminished reduction of oxyhemoglobin, then, there should be a parallel decrease in alveolar and CSF PCO 〈 sub 〉 2 〈 /sub 〉 during O 〈 sub 〉 2 〈 /sub 〉 breathing in neonates. To test this hypothesis, we measured ventilation, alveolar PCO 〈 sub 〉 2 〈 /sub 〉 and CSF PCO 〈 sub 〉 2 〈 /sub 〉 , pH and HCO 〈 sub 〉 2 〈 /sub 〉 before and 10–20 min after infants began breathing 100% O 〈 sub 〉 2 〈 /sub 〉 . With 100% O 〈 sub 〉 2 〈 /sub 〉 , minute ventilation increased from 0.193 ± (SE) 0.013 (n = 7) to 0.252 ± 0.013 liter/min/kg (p 〈 0.015), P 〈 sub 〉 A 〈 /sub 〉 CO 〈 sub 〉 2 〈 /sub 〉 decreased from 42 ± 2 to 38 ± 2 mm Hg (p 〈 0.005), CSF PCO 〈 sub 〉 2 〈 /sub 〉 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 PCO 〈 sub 〉 2 〈 /sub 〉 at the central level.
Materialart:
Online-Ressource
ISSN:
1661-7800
,
1661-7819
Sprache:
Englisch
Verlag:
S. Karger AG
Publikationsdatum:
1980
ZDB Id:
2403535-X
SSG:
12
