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The carotid body and arousal in the fetus and neonate
1Department of Pediatrics, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756, United States. robert.a.darnall@dartmouth.edu
Insights
Infant arousal failure during sleep may contribute to Sudden Infant Death Syndrome (SIDS). This review explores how hypoxia and carbon dioxide impact infant arousal, focusing on the carotid body
Area of Science:
- Neuroscience
- Pediatrics
- Respiratory Physiology
Background:
- Arousal from sleep is a critical defense mechanism in infants against hypoxia and hypercapnia.
- Arousal failure is a potential contributor to Sudden Infant Death Syndrome (SIDS).
- Brainstem abnormalities in SIDS infants are often linked to the arousal process.
Purpose of the Study:
- To review the role of arousal mechanisms in fetal and newborn responses to hypoxia and carbon dioxide.
- To examine the involvement of the carotid body (CB) in infant arousal.
- To identify current knowledge gaps regarding specific arousal pathways.
Main Methods:
- Review of existing literature on infant arousal, hypoxia, hypercapnia, and the carotid body.
- Analysis of sleep state-dependent arousal patterns (AS vs. QS) in mammals and human infants.
- Discussion of potential neurochemical mechanisms, including GABAergic pathways and chemoreceptors.
Main Results:
- Arousal is suppressed during active sleep (AS) in human infants, unlike most mammals.
- Repeated hypoxia exposure can blunt arousal, potentially via medullary raphe GABAergic mechanisms.
- Carotid body (CB) chemoreceptors are crucial for hypoxic arousal; central chemoreceptors are implicated in CO2 arousal.
Conclusions:
- The carotid body plays a significant role in mediating arousal responses to hypoxia in newborns.
- The precise pathways linking CB stimulation to arousal centers, directly or indirectly, require further investigation.
- Understanding these mechanisms is vital for addressing arousal deficits potentially linked to SIDS.
Abstract:
Arousal from sleep is a major defense mechanism in infants against hypoxia and/or hypercapnia. Arousal failure may be an important contributor to SIDS. Areas of the brainstem that have been found to be abnormal in a majority of SIDS infants are involved in the arousal process. Arousal is sleep state dependent, being depressed during AS in most mammals, but depressed during QS in human infants. Repeated exposure to hypoxia causes a progressive blunting of arousal that may involve medullary raphe GABAergic mechanisms. Whereas CB chemoreceptors contribute heavily to arousal in response to hypoxia, serotonergic central chemoreceptors have been implicated in the arousal response to CO(2). Pulmonary or chest wall mechanoreceptors also contribute to arousal in proportion to the ventilatory response and decreases in their input may contribute to depressed arousal during AS. Little is known about specific arousal pathways beyond the NTS. Whether CB chemoreceptor stimulation directly stimulates arousal centers or whether this is done indirectly through respiratory networks remains unknown. This review will focus on arousal in response to hypoxia and CO(2) in the fetus and newborn and will outline what we know (and do not know) about the involvement of the carotid body in this process.
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