Reid G M
Te Aroha, New Zealand.
Med Hypotheses. 2001 Mar;56(3):280-5. doi: 10.1054/mehy.2000.1275.
Sudden infant death syndrome (SIDS) has been described as a silent unexpected death during sleep. Infants with near-miss SIDS have shown a higher heart rate and diminished heart rate variability during sleep. Non-rapid-eye-movement (NREM) sleep rate variability was related to respiration. A decreased heart rate variability was also observed in infants with respiratory distress syndrome (RDS) or prenatal hypoxia. It was hypothesized that decreased heart rate variability and decreased body measurement during sleep were related to a decreased arousal response. Cardiac output is greater in the supine position. Acetylcholine slows the heart beat. Postural changes modify the acute baroreflex control of the heart rate. The cerebellum also contributes to the reflex anti-orthostatic (supine) cardiovascular response to postural change. Delayed myelination of various areas of the brain occurred in SIDS victims and it was suggested that the defect in central respiratory control could be a motor rather than a sensory problem, and that the search for abnormalities should be extended to regions in the cerebellum and pre-frontal-temporal-limbic systems. The cerebellum exercises control over motor neuron impulses from the cerebral cortex to lower structures. An extended period of neonatal decreased body movement has its counterpart in the astronaut exposed to the deconditioning effect of zero gravity. Hypodynamia induces hyperglycemia, insulin resistance, renal inositoluria and impaired nerve conduction. Myoinositol is 20 times higher in fetal-like tissue than in adults. The insecticide lindane (gammexane) is an inositol antagonist. Lindane administration to neonatal rats induced low levels of specific components of myelin proteins in oligodendrocytes in the brain. The activity of these specific enzymes was reduced in oligodendrocytes in the brain of SIDS victims. It is hypothesized that lindane administration to laboratory neonatal animals is a laboratory model for studying delayed development of the brain in SIDS.
婴儿猝死综合征(SIDS)被描述为睡眠期间意外发生的无声死亡。接近SIDS的婴儿在睡眠期间心率较高且心率变异性降低。非快速眼动(NREM)睡眠心率变异性与呼吸有关。在患有呼吸窘迫综合征(RDS)或产前缺氧的婴儿中也观察到心率变异性降低。据推测,睡眠期间心率变异性降低和身体测量值下降与唤醒反应降低有关。仰卧位时心输出量更大。乙酰胆碱会减慢心跳。姿势改变会改变心率的急性压力反射控制。小脑也有助于对姿势改变产生反射性抗直立位(仰卧位)心血管反应。SIDS受害者大脑的各个区域出现髓鞘形成延迟,有人提出中枢呼吸控制缺陷可能是运动问题而非感觉问题,对异常情况的搜索应扩展到小脑和前额叶 - 颞叶 - 边缘系统区域。小脑对从大脑皮层到较低结构的运动神经元冲动进行控制。新生儿长时间身体活动减少与暴露于零重力去适应效应的宇航员情况类似。动力不足会导致高血糖、胰岛素抵抗、肾肌醇尿症和神经传导受损。胎儿样组织中的肌醇比成人高20倍。杀虫剂林丹(γ - 六氯环己烷)是一种肌醇拮抗剂。给新生大鼠施用林丹会导致其大脑少突胶质细胞中髓鞘蛋白的特定成分水平降低。这些特定酶的活性在SIDS受害者大脑的少突胶质细胞中降低。据推测,给实验室新生动物施用林丹是研究SIDS中大脑发育延迟的实验室模型。