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外周动脉化学感受器与婴儿猝死综合征

Peripheral arterial chemoreceptors and sudden infant death syndrome.

作者信息

Gauda Estelle B, Cristofalo Elizabeth, Nunez Jeanne

机构信息

Department of Pediatrics, Division of Neonatology, Johns Hopkins Medical Institutions, Johns Hopkins Hospital, Baltimore, MD 21287-3200, USA.

出版信息

Respir Physiol Neurobiol. 2007 Jul 1;157(1):162-70. doi: 10.1016/j.resp.2007.02.016. Epub 2007 Mar 2.

Abstract

Sudden infant death syndrome (SIDS) is the major cause of death in infants between 1 month and 1 year of age. Two particular concerns are that (1) premature or low birth weight (<2500-g) infants have a 2- to 40-fold greater risk of dying of SIDS (depending on the sleep position) than infants born at term and of normal birth weight, and that (2) the proportion of premature infants dying of SIDS has increased from 12 to 34% between 1988 and 2003. Hypo- and hypersensitivity of peripheral arterial chemoreceptors (PACs) may be one biological mechanism that could help to explain the epidemiological association between the increased incidence of SIDS in formerly premature infants. Because premature infants are often exposed to the extremes of oxygen stress during early postnatal development, they are more likely to have a maladaptive response of PACs later in their lives. As the first line of defense that mediates an increase in ventilation to a hypoxic challenge during wakefulness and sleep, PACs also mediate arousal responses during sleep in response to an asphyxial event that is often associated with upper airway obstruction. In most mammalian species, PACs are not fully developed at birth and thus are vulnerable to plasticity-induced changes mediated by environmental exposures such as the extremes of oxygen tension. Hypoxic or hyperoxic exposure during early postnatal development can lead to hyposensitive or hypersensitive PAC responses later in life. Although baseline chemoreceptor activity may not be the cause of an initial hypoxic or asphyxial event, the level of peripheral chemoreceptor drive does modulate the (1) time to arousal, (2) resumption of airflow during airway obstruction, (3) escape behaviors during rebreathing, and (4) cardiorespiratory responses that result from activation of the laryngeal chemoreflex. The laryngeal chemoreflex can be stimulated by reflux of gastric contents above the upper esophageal sphincter, or an increase in nasopharyngeal secretions from upper respiratory tract infections--events that contribute to some cases of SIDS. In this review, evidence is presented that both hypo- and hypersensitivity of PACs may be disadvantageous to the premature infant who is placed in an at risk environment for the occurrence of hypoxemia/asphyxia event thereby predisposing the infant to SIDS.

摘要

婴儿猝死综合征(SIDS)是1个月至1岁婴儿死亡的主要原因。两个特别值得关注的问题是:(1)早产或低出生体重(<2500克)婴儿死于SIDS的风险比足月儿和正常出生体重婴儿高2至40倍(取决于睡眠姿势);(2)1988年至2003年间,死于SIDS的早产儿比例从12%增至34%。外周动脉化学感受器(PACs)的低敏和高敏可能是一种生物学机制,有助于解释既往早产儿中SIDS发病率增加之间的流行病学关联。由于早产儿在出生后早期发育过程中常暴露于极端的氧应激环境,他们在日后生活中更有可能出现PACs的适应不良反应。作为在清醒和睡眠期间介导对低氧挑战通气增加的第一道防线,PACs在睡眠期间也介导对常与上呼吸道阻塞相关的窒息事件的觉醒反应。在大多数哺乳动物物种中,PACs在出生时并未完全发育,因此易受环境暴露(如极端氧张力)介导的可塑性诱导变化的影响。出生后早期发育期间的低氧或高氧暴露可导致日后生活中PAC反应低敏或高敏。虽然基线化学感受器活动可能不是初始低氧或窒息事件的原因,但外周化学感受器驱动水平确实会调节:(1)觉醒时间;(2)气道阻塞期间气流的恢复;(3)再呼吸期间的逃避行为;(4)由喉化学反射激活引起的心肺反应。喉化学反射可由胃内容物反流至上食管括约肌上方或上呼吸道感染引起的鼻咽分泌物增加所刺激——这些事件导致了一些SIDS病例。在本综述中,有证据表明,PACs的低敏和高敏对处于发生低氧血症/窒息事件风险环境中的早产儿可能都不利,从而使婴儿易患SIDS。

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