Document Detail


Maturation of peripheral arterial chemoreceptors in relation to neonatal apnoea.
MedLine Citation:
PMID:  15050211     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Apnoea and periodic breathing are the hallmarks of breathing for the infant who is born prematurely. Sustained respiration is obtained through modulation of respiratory-related neurons with inputs from the periphery. The peripheral arterial chemoreceptors, uniquely and reflexly change ventilation in response to changes in oxygen tension. The chemoreflex in response to hypoxia is hyperventilation, bradycardia and vasoconstriction. The fast response time of the peripheral arterial chemoreceptors to changes in oxygen and carbon dioxide tension increases the risk of more periodicity in the breathing pattern. As a result of baseline hypoxaemia, peripheral arterial chemoreceptors contribute more to baseline breathing in premature than in term infants. While premature infants may have an augmented chemoreflex, infants who develop bronchopulmonary dysplasia have a blunted chemoreflex at term gestation. The development of chemosensitivity of the peripheral arterial chemoreceptors and environmental factors that might cause maldevelopment of chemosensitivity with continued maturation are reviewed in an attempt to help explain the physiology of apnoea of prematurity and the increased incidence of sudden infant death syndrome (SIDS) in infants born prematurely and those who are exposed to tobacco smoke.
Authors:
Estelle B Gauda; Gabrielle L McLemore; Jose Tolosa; Jannette Marston-Nelson; Daniel Kwak
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Seminars in neonatology : SN     Volume:  9     ISSN:  1084-2756     ISO Abbreviation:  Semin Neonatol     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-03-30     Completed Date:  2004-09-14     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9606001     Medline TA:  Semin Neonatol     Country:  England    
Other Details:
Languages:  eng     Pagination:  181-94     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD 21287-3200, USA. egauda@jhmi.edu
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MeSH Terms
Descriptor/Qualifier:
Anoxia / physiopathology
Apnea / physiopathology*
Arteries / physiology*
Carotid Body / physiology
Chemoreceptor Cells / anatomy & histology,  physiology*
Dopamine / physiology
Humans
Incidence
Infant, Newborn
Infant, Premature
Infant, Premature, Diseases / physiopathology*
Nicotine / adverse effects
Oxygen / analysis
Respiratory Physiological Phenomena
Risk Factors
Sudden Infant Death / epidemiology,  etiology
Tobacco Smoke Pollution / adverse effects
Grant Support
ID/Acronym/Agency:
R01 DA13940/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/Tobacco Smoke Pollution; 54-11-5/Nicotine; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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