A neonatal mouse model of intermittent hypoxia associated with features of apnea in premature infants

被引:38
作者
Cai, Jun [1 ,2 ]
Tuong, Chi Minh [1 ]
Gozal, David [3 ]
机构
[1] Univ Louisville, Sch Med, Dept Pediat, Kosair Childrens Hosp,Res Inst, Louisville, KY 40202 USA
[2] Univ Louisville, Sch Med, Dept Anat Sci & Neurobiol, Louisville, KY 40202 USA
[3] Univ Chicago, Pritzker Sch Med, Dept Pediat, Comer Childrens Hosp, Chicago, IL 60637 USA
关键词
Mouse model; Intermittent hypoxia; Infantile apnea; Apnea of prematurity; White matter; OBSTRUCTIVE SLEEP-APNEA; CENTRAL HYPOVENTILATION SYNDROME; WHITE-MATTER INJURY; PRETERM INFANTS; VENTILATORY RESPONSE; AIRWAY OBSTRUCTIONS; BRAIN-DEVELOPMENT; CHRONIC CONSTANT; GENE-EXPRESSION; C57BL/6J MOUSE;
D O I
10.1016/j.resp.2011.06.003
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
A neonatal mouse model of intermittent hypoxia (IH) simulating the recurring hypoxia/reoxygenation episodes of apnea of prematurity (AOP) was developed. C57BL/6 P2 pups were culled for exposure to either intermittent hypoxia or intermittent air as control. The IH paradigms consisted of alternation cycles of 20.9% O(2) and either 8.0% or 5.7% O(2) every 120 or 140s for 6 ha day during daylight hours from day 2 to day 10 postnatally. i.e., roughly equivalent to human brain development in the perinatal period. IH exposures elicited modest to severe decrease in oxygen saturation along with bradycardia in neonatal mice, which were severity-dependent. Hypomyelination in both central and peripheral nervous systems was observed despite the absence of visible growth retardation. The neonatal mouse model of IH in this study partially fulfills the current diagnostic criteria with features of AOP, and provides opportunities to reproduce in rodents some of the pathophysiological changes associated with this disorder, such as alterations in myelination. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:210 / 217
页数:8
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