Sudden infant death syndrome: a theory.
Sudden infant death syndrome: a theory.
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婴儿猝死综合症：一种理论。
DOI：
10.1016/s0149-7634(05)80014-4
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发表时间：
1993
影响因子：
8.2
通讯作者：
Perry,GW
中科院分区：
文献类型：
--
作者：
Vertes,RP;Perry,GW
婴儿猝死综合征（SIDS）的一个假设，并支持证据。我们的模型如下。SIDS婴儿的胎儿血红蛋白水平异常升高，这会导致慢性缺氧状态。慢性缺氧在慢波睡眠（一种正常的呼吸抑制状态）期间对呼吸系统产生明显的抑制作用。这些抑郁的影响在婴儿2-4个月大的发育期尤其明显，在这一时期，慢波睡眠开始占据婴儿总睡眠时间的很大比例。在慢波睡眠中开始向下螺旋，使得缺氧诱导的通气减少产生更极端的缺氧，导致进一步的呼吸抑制，并最终由于呼吸停止而死亡。
A hypothesis, and supporting evidence, is presented for the sudden infant death syndrome (SIDS). Our model is as follows. Fetal hemoglobin levels are abnormally elevated in SIDS infants, which contributes to a state of chronic hypoxia. Chronic hypoxia produces pronounced depressive effects on the respiratory system during slow wave sleep (a state of normal respiratory depression). These depressive effects are particularly manifest during that period of development in which slow wave sleep begins to occupy a very large percentage of total sleep time in infants — 2–4 mo of age. A downward spiral is initiated in slow wave sleep such that hypoxia-induced decreases in ventilation produce more extreme hypoxia leading to further respiratory depression and ultimately death due to a cessation of respiration.