Predominant role of peripheral chemoreceptors in the termination of apnea in maturing newborn lambs.
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 varying inspired O2 fraction levels. The apnea termination threshold PCO2 (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 at both 1 and 15 days of life, 2) intact 1-day-old lambs with central tissue hypoxia induced by CO inhalation, and 3) 1-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 that was a determinant for the termination of an apnea. PATTCO2 invariably increased when arterial PO2 increased, regardless of age. During hypoxia and normoxia, PATTCO2 was significantly lower in 15-day-old lambs compared with 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 a low inspired O2 fraction 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.
Delacourt
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Jeremy Rill Center and Pulmonary Research Center, Department of Pediatrics, Sherbrooke University, Quebec, Canada.
Canet
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Bureau
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D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D001049:Apnea / Q000503:physiopathology*; D002248:Carbon Monoxide / Q000494:pharmacology*; D002628:Chemoreceptor Cells / Q000502:physiology*; D006985:Hyperventilation; D000860:Hypoxia / Q000503:physiopathology; D010100:Oxygen / Q000494:pharmacology*; D012767:Ships
D002248:Carbon Monoxide; D010100:Oxygen