Sleep influences on homeostatic functions: implications for sudden infant death syndrome
Sleep influences on homeostatic functions: implications for sudden infant death syndrome
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DOI：
10.1016/s0034-5687(99)00107-3
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发表时间：
2000-02-01
期刊：
影响因子：
--
通讯作者：
Thach, BT
中科院分区：
文献类型：
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作者：
Harper, RM;Kinney, HC;Thach, BT
婴儿猝死综合症（SIDS）的潜在机制似乎起源于胎儿环境，导致神经损伤，进而损害睡眠期间对呼吸或血压挑战的反应。这些缺陷似乎涉及化学感受和心血管控制区域内神经递质受体的改变。 SIDS 风险会因产前和产后接触尼古丁以及可能因缺氧经历而增加。俯卧的睡姿在风险中起着重要作用，尽量减少面部从封闭空间逃逸的头部姿势也是如此；体温升高也可能是一个因素。补偿机制，包括喘息能力减弱、相对无法唤醒到更安全的状态，或者无法调动呼吸努力来克服血压下降，一直是最近研究工作的目标。研究结果表明，致命事件涉及神经受损的婴儿，这种情况对重要的生理机能提出了挑战，最有可能是在睡眠期间，在特定的发育时期。 (C) 2000 Elsevier Science B.V. 保留所有权利。
The mechanisms underlying the sudden infant death syndrome (SIDS) appear to have origins in the fetal environment resulting in neural damage which later compromises responses to breathing or blood pressure challenges during sleep. The deficits appear to involve alterations in neurotransmitter receptors within regions involved in chemoreception and cardiovascular control. SIDS risk is enhanced by pre- and postnatal nicotine exposure, and possibly by hypoxic experiences. The prone sleeping position plays a significant role in risk, as do head positions that minimize facial escape from enclosed spaces; elevated body temperature may also be a factor. Compensatory mechanisms, including diminished gasping ability, relative failure to arouse to a safer state, or a failure to recruit respiratory efforts to overcome a blood pressure loss have been the object of recent research efforts. The findings suggest that the fatal event involves a neurally-compromised infant, circumstances that challenge vital physiology, most likely during sleep, at a particular developmental period. (C) 2000 Elsevier Science B.V. All rights reserved.