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Published on: November 20, 2015
Premature birth, homeostatic plasticity and respiratory consequences of inflammation
Estelle B Gauda1, Gabrielle L McLemore2
1The Hospital for Sick Children, Division of Neonatology, Department of Pediatrics, University of Toronto, Toronto, Ontario, M5G 1X8, Canada.
Insights
Premature birth can disrupt infant respiratory control, leading to breathing issues. This review explores how early birth triggers lasting changes in the respiratory network, increasing risks like apnea and SIDS.
Area of Science:
- Neonatology
- Neuroscience
- Respiratory Physiology
Background:
- Premature infants face risks like persistent apnea, SIDS, and sleep-disordered breathing.
- Autonomic nervous system development, crucial for breathing control, occurs late in gestation.
- Modern neonatology enables survival of extremely premature infants, with significant respiratory system maturation happening outside the womb.
Purpose of the Study:
- To review the impact of premature birth on respiratory control mechanisms.
- To explore the concept of homeostatic plasticity in the developing respiratory network.
- To discuss the link between premature birth, plasticity, and respiratory depression during inflammation.
Main Methods:
- Literature review focusing on premature birth, autonomic nervous system development, and respiratory control.
- Analysis of homeostatic plasticity as a mechanism for altered respiratory network output.
- Discussion of biological pathways involved in respiratory depression in former premature infants.
Main Results:
- Early birth during the last trimester may induce persistent inhibitory plasticity in the respiratory network.
- This plasticity can lead to ongoing breathing regulation issues in infancy and childhood.
- Inflammation can exacerbate respiratory depression in former premature infants due to these altered mechanisms.
Conclusions:
- Premature birth can fundamentally alter the developing respiratory neural network.
- Homeostatic plasticity is a key mechanism explaining persistent respiratory dysfunction in ex-utero maturation.
- Understanding these mechanisms is crucial for managing respiratory risks in premature infants.
Abstract:
Infants who are born premature can have persistent apnea beyond term gestation, reemergence of apnea associated with inflammation during infancy, increased risk of sudden unexplained death, and sleep disorder breathing during infancy and childhood. The autonomic nervous system, particularly the central neural networks that control breathing and peripheral and central chemoreceptors and mechanoreceptors that modulate the activity of the central respiratory network, are rapidly developing during the last trimester (22-37 weeks gestation) of fetal life. With advances in neonatology, in well-resourced, developed countries, infants born as young as 23 weeks gestation can survive. Thus, a substantial part of maturation of central and peripheral systems that control breathing occurs ex-utero in infants born at the limit of viability. The balance of excitatory and inhibitory influences dictates the ultimate output from the central respiratory network. We propose in this review that simply being born early in the last trimester can trigger homeostatic plasticity within the respiratory network tipping the balance toward inhibition that persists in infancy. We discuss the intersection of premature birth, homeostatic plasticity and biological mechanisms leading to respiratory depression during inflammation in former premature infants.
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