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Pathophysiology of Childhood Obstructive Sleep Apnea

Pathophysiology of Childhood Obstructive Sleep Apnea
儿童阻塞性睡眠呼吸暂停的病理生理学
批准号:
6544430
负责人:
CAROLE L MARCUS
金额:
$32.7万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1998
资助国家:
美国
项目状态:
已结题
起止时间:
1998-07-06 至 2003-06-30

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英文摘要
DESCRIPTION (provided by applicant): The obstructive sleep apnea syndrome (OSAS) is a common cause of morbidity in childhood. However, its pathophysiology is poorly understood. It is hypothesized that changes in upper airway neuromotor tone during development play a major role in the maintenance of upper airway patency during sleep, and the expression of sleep-disordered breathing. The following hypotheses will be tested during sleep: (1) That, in normal subjects, upper airway collapsibility is lowest during childhood and increases with age, with a critical transition occurring during adolescence. The decreased collapsibility noted during childhood is due primarily to increased upper airway reflex neuromotor tone. Specifically, in normal, non-snoring subjects, we will (a) Establish baseline differences in UA function between children and adults in the hypotonic condition; (b) Examine the effects of UA reflexes on UA patency in normal children compared to adults, and (c) Determine the effect of puberty on UA collapsibility. (2) That OSAS develops in children lacking these protective upper airway reflexes. Specifically, in normal children compared to children with OSAS, we will (a) Establish baseline differences in UA function in the hypotonic condition, (b) Determine the role of REM sleep on UA collapsibility, and (c) Examine the effects of UA reflexes on UA patency. (3) That regulation of neuromotor tone, and the central response to an upper airway load, accounts for the polysomnographic characteristics of sleep-disordered breathing unique to childhood OSAS. Specifically, we will (a) Examine the effects of UA reflexes on UA patency in children with obstructive hypoventilation (OH) vs children with discrete, cyclical obstructive apneas (OA), (b) Measure the arousal threshold to an inspiratory resistive load in children with OH vs OA, and (c) Measure the respiratory-related evoked potentials (RREP) in response to inspiratory occlusion during sleep in children with OA vs OH and controls. These studies will help elucidate the underlying pathophysiology of childhood OSAS, resulting in better understanding and improved management of this disease.
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