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Published on: October 25, 2019
Carotid chemoreceptor development and neonatal apnea
Peter M MacFarlane1, Ana P Ribeiro, Richard J Martin
1Case Western Reserve University, Rainbow Babies & Children's Hospital, 11100 Euclid Avenue, Cleveland, OH 44106-6010, USA. peter.macfarlane@case.edu
Insights
Carotid chemoreceptors influence neonatal apnea by affecting breathing control. Xanthine therapy may help prevent apnea in preterm infants with immature respiratory systems.
Area of Science:
- Neonatal physiology
- Respiratory control
- Neuroscience
Background:
- Preterm infants have immature respiratory control, leading to apnea and intermittent hypoxia (IH).
- Carotid chemoreceptors are implicated in apnea but their precise role in initiation and termination is unclear.
- Postnatal maturation of carotid chemoreceptors correlates with reduced hypoxemic events.
Purpose of the Study:
- To review the role of carotid chemoreceptors in neonatal apnea initiation and termination.
- To discuss the potential protective role of carotid chemoreceptor sensitization.
- To explore xanthine therapy for apnea prevention in neonates.
Main Methods:
- Literature review of neonatal respiratory control and carotid chemoreceptor function.
- Analysis of studies on intermittent hypoxia and chemoreceptor sensitization in animal models.
- Examination of clinical data on apnea and xanthine therapy.
Main Results:
- Carotid chemoreceptor input is a significant factor in neonatal apnea.
- Chronic intermittent hypoxia may sensitize carotid chemoreceptors, potentially perpetuating or protecting against apnea.
- Xanthine therapy is a potential treatment for preventing apnea.
Conclusions:
- Carotid chemoreceptors play a complex role in neonatal apnea, influencing both its onset and resolution.
- Further research is needed to fully elucidate the dual role of chemoreceptor sensitization.
- Xanthine therapy shows promise for managing apnea in preterm infants.
Abstract:
The premature transition from fetal to neonatal life is accompanied by an immature respiratory neural control system. Most preterm infants exhibit recurrent apnea, resulting in repetitive oscillations in O(2) saturation (intermittent hypoxia, IH). Numerous factors are likely to play a role in the etiology of apnea including inputs from the carotid chemoreceptors. Despite major advances in our understanding of carotid chemoreceptor function in the early neonatal period, however, their contribution to the initiation of an apneic event and its eventual termination are still largely speculative. Recent findings have provided a detailed account of the postnatal changes in the incidence of hypoxemic events associated with apnea, and there is anecdotal evidence for a positive correlation with carotid chemoreceptor maturation. Furthermore, studies on non-human animal models have shown that chronic IH sensitizes the carotid chemoreceptors, which has been proposed to perpetuate the occurrence of apnea. An alternative hypothesis is that sensitization of the carotid chemoreceptors could represent an important protective mechanism to defend against severe hypoxemia. The purpose of this review, therefore, is to discuss how the carotid chemoreceptors may contribute to the initiation and termination of an apneic event in the neonate and the use of xanthine therapy in the prevention of apnea.
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