Premium
The impact of preterm adversity on cardiorespiratory function
Author(s) -
McDonald Fiona B.,
Dempsey Eugene M.,
O'Halloran Ken D.
Publication year - 2019
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep087490
Subject(s) - cardiorespiratory fitness , hyperoxia , hypoxia (environmental) , context (archaeology) , oxygen tension , homeostasis , immune system , medicine , physiology , psychology , immunology , biology , oxygen , lung , paleontology , chemistry , organic chemistry
New FindingsWhat is the topic of this review? We review the influence of prematurity on the cardiorespiratory system and examine the common sequel of alterations in oxygen tension, and immune activation in preterm infants.What advances does it highlight? The review highlights neonatal animal models of intermittent hypoxia, hyperoxia and infection that contribute to our understanding of the effect of stress on neurodevelopment and cardiorespiratory homeostasis. We also focus on some of the important physiological pathways that have a modulatory role on the cardiorespiratory system in early life.Abstract Preterm birth is one of the leading causes of neonatal mortality. Babies that survive early‐life stress associated with immaturity have significant prevailing short‐ and long‐term morbidities. Oxygen dysregulation in the first few days and weeks after birth is a primary concern as the cardiorespiratory system slowly adjusts to extrauterine life. Infants exposed to rapid alterations in oxygen tension, including exposures to hypoxia and hyperoxia, have altered redox balance and active immune signalling, leading to altered stress responses that impinge on neurodevelopment and cardiorespiratory homeostasis. In this review, we explore the clinical challenges posed by preterm birth, followed by an examination of the literature on animal models of oxygen dysregulation and immune activation in the context of early‐life stress.