Abstract

In previous studies we examined the development of the response of carotid and aortic chemoreceptors to hypoxia in the lamb and kitten (Blanco et al, 1984; Hanson et al, 1989; Kumar & Hanson, 1989). Recently we have been examining the question of whether the response of the arterial chemoreceptors to CO2 also develops post-natally. The issue is important because, whilst elevation in arterial PCO2 (PaCO2) stimulates fetal chemoreceptors and fetal breathing movements, the effect of rapid changes in PaCO2 on chemoreceptors in the neonate is largely unknown. Because CO2 production is linked to metabolism, it provides an important component of the drive to breathe in the neonate, especially at an age when the response to hypoxia is poor. This might be an important consideration in apnoea and respiratory failure in the neonate. Environmental temperature will, of course, affect metabolism and overheating has been proposed to play a role in the aetiology of certain types of respiratory failure, including sudden infant death syndrome. In previous studies (Watanabe et al, 1993) we found that environmental temperatures affected the gain of respiratory chemoreflex responses to changes in PaO2 and PaCO2. However, without direct information on chemoreceptor responses to CO2, the mechanisms underlying such effects cannot be determined. For this reason we embarked on a study of the maturation of carotid chemoreceptor responses to CO2 in the lamb. Preliminary data on the maturation of steady state and dynamic responses to CO2 has already been published (Calder et al, 1995). In this report we concentrate on the adaptive nature of the chemoreceptor response to CO2.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call