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Published on: August 19, 2020
Peripheral arterial chemoreceptors and sudden infant death syndrome
Estelle B Gauda1, Elizabeth Cristofalo, Jeanne Nunez
1Department of Pediatrics, Division of Neonatology, Johns Hopkins Medical Institutions, Johns Hopkins Hospital, Baltimore, MD 21287-3200, USA. egauda@jhmi.edu
Insights
Sudden infant death syndrome (SIDS) risk is higher in premature infants. Impaired peripheral arterial chemoreceptors (PACs) may explain this increased SIDS risk in vulnerable infants.
Area of Science:
- Neonatal physiology
- Respiratory control
- Sudden Infant Death Syndrome (SIDS) research
Background:
- Sudden infant death syndrome (SIDS) is a leading cause of infant mortality, disproportionately affecting premature and low birth weight infants.
- Premature infants face increased SIDS risk due to potential maladaptive responses in peripheral arterial chemoreceptors (PACs) following early-life oxygen stress.
- PACs are crucial for mediating ventilation, arousal, and cardiorespiratory responses to hypoxia and airway obstruction, and are vulnerable to environmental influences during development.
Purpose of the Study:
- To explore the potential role of peripheral arterial chemoreceptor (PAC) hypo- and hypersensitivity in the increased incidence of SIDS among premature infants.
- To review the biological mechanisms linking PAC dysfunction to SIDS risk in at-risk infant populations.
Main Methods:
- Review of existing epidemiological and physiological evidence.
- Analysis of the role of PACs in cardiorespiratory control and arousal mechanisms.
- Examination of the impact of early-life oxygen exposure on PAC development and function.
Main Results:
- Premature infants exhibit a higher risk of SIDS, with a notable increase in the proportion of SIDS deaths attributed to this group.
- Hypo- or hypersensitivity of PACs, potentially resulting from early-life oxygen stress, may impair arousal and cardiorespiratory responses to asphyxial events.
- PAC dysfunction can negatively impact responses to laryngeal chemoreflex activation, which may be triggered by events like gastric reflux or infections.
Conclusions:
- Peripheral arterial chemoreceptor (PAC) dysfunction (both hypo- and hypersensitivity) is a plausible biological mechanism contributing to the elevated SIDS risk in premature infants.
- Environmental factors affecting PAC development in premature infants may predispose them to SIDS.
- Further research into PAC function in premature infants is warranted to understand and potentially mitigate SIDS risk.
Abstract:
Sudden infant death syndrome (SIDS) is the major cause of death in infants between 1 month and 1 year of age. Two particular concerns are that (1) premature or low birth weight (<2500-g) infants have a 2- to 40-fold greater risk of dying of SIDS (depending on the sleep position) than infants born at term and of normal birth weight, and that (2) the proportion of premature infants dying of SIDS has increased from 12 to 34% between 1988 and 2003. Hypo- and hypersensitivity of peripheral arterial chemoreceptors (PACs) may be one biological mechanism that could help to explain the epidemiological association between the increased incidence of SIDS in formerly premature infants. Because premature infants are often exposed to the extremes of oxygen stress during early postnatal development, they are more likely to have a maladaptive response of PACs later in their lives. As the first line of defense that mediates an increase in ventilation to a hypoxic challenge during wakefulness and sleep, PACs also mediate arousal responses during sleep in response to an asphyxial event that is often associated with upper airway obstruction. In most mammalian species, PACs are not fully developed at birth and thus are vulnerable to plasticity-induced changes mediated by environmental exposures such as the extremes of oxygen tension. Hypoxic or hyperoxic exposure during early postnatal development can lead to hyposensitive or hypersensitive PAC responses later in life. Although baseline chemoreceptor activity may not be the cause of an initial hypoxic or asphyxial event, the level of peripheral chemoreceptor drive does modulate the (1) time to arousal, (2) resumption of airflow during airway obstruction, (3) escape behaviors during rebreathing, and (4) cardiorespiratory responses that result from activation of the laryngeal chemoreflex. The laryngeal chemoreflex can be stimulated by reflux of gastric contents above the upper esophageal sphincter, or an increase in nasopharyngeal secretions from upper respiratory tract infections--events that contribute to some cases of SIDS. In this review, evidence is presented that both hypo- and hypersensitivity of PACs may be disadvantageous to the premature infant who is placed in an at risk environment for the occurrence of hypoxemia/asphyxia event thereby predisposing the infant to SIDS.
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