Predominant role of peripheral chemoreceptors in the termination of
apnea in maturing newborn lambs.
Delacourt, Christophe, Emmanuel Canet, and Michel A. Bureau.
Jeremy Rill Center and Pulmonary Research Center, Department of
Pediatrics, Sherbrooke University, Sherbrooke, Quebec J1H 5N4,
Canada
APStracts 2:0480A, 1995.
Apneas are very common and normal in newborns but may become life
-threatening if they are not terminated appropriately. The aim of this
study in newborn lambs was to investigate the influence on apnea
termination of postnatal maturation, peripheral chemoreceptor
function, and hypoxia. Apneas were induced by passive
hyperventilation at various FIO2 levels. The PCO2 apnea termination
threshold (PATTCO2) was defined as the arterial PCO2 value at the
first breath after the apnea. Three groups of awake intubated lambs
were studied: 1) intact lambs tested both at one day and 15 days of
life ; 2) intact one-day-old lambs with central tissue hypoxia
induced by CO inhalation ; 3) one-day-old lambs with carotid body
denervation (CBD). In individual lambs and regardless of age and
carotid body function, there was a PO2/PCO2 response curve which was
determinant for the termination of an apnea. PATTCO2 invariably
increased when PaO2 increased, regardless of age. During hypoxia and
normoxia, PATTCO2 was significantly lower in 15-day-old lambs as
compared to 1-day-old lambs. No difference was seen during hyperoxia.
PATTCO2 values were shifted to higher levels after carotid body
removal. Finally, hypoxia induced by either low FIO2 or CO inhalation
consistently failed to induce a depressive effect on the PATTCO2,
even in CBD lambs. In conclusion, in awake newborn lambs, the PCO2
level for apnea termination changed with postnatal age, and carotid
body function was essential in lowering PATTCO2, thus protecting the
lambs against prolonged apnea. Furthermore, hypoxia consistently
failed to depress the reinitiation of breathing after apnea, even in
CBD lambs.
Received 13 December 1994; accepted in final form 19 October
1995.
APS Manuscript Number A1269-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95