CARDIORESPIRATORY & AUTONOMIC RESPONSES TO AROUSAL FROM SLEEP

频谱分析在心率数据采集中的应用 宫内暴露于可卡因的婴儿和正常对照 睡眠状态对心率变异性有显著影响， 与活跃睡眠相比，安静睡眠（QS）期间观察到的频率功率 (AS)AS的低频和中频功率大于 QS。 然而，在两种睡眠状态下，可卡因暴露的新生儿 显示出增强的总光谱功率，这似乎是由于 在所有频带上的频谱功率增加。 绝对 HRV中低频带的频谱功率值 在可卡因暴露组中， states. 高频功率的绝对值也较高， 但这种增加仅在安静的情况下达到统计学显著性， 睡吧 我们没有发现呼吸模式差异的证据 这两个群体之间的差异可能会解释这些发现。 非常 QS和AS的总呼吸变异性在 低频到中频范围，这表明周期性呼吸 在相同的频率范围内对HRV的贡献很小。 我们也 计算了心率变化的分数分布， 所有频率作为检查交感迷走神经平衡的手段。 比率 低频和中频功率与高频功率相比 两组之间没有差异，尽管有很高的 与QS相比，AS显著增加。 目前的结果 提出两种可能性：（1）副交感神经控制增强 （2）可卡因暴露婴儿的心率增加;或 迷走神经和交感神经对心率的调节 可卡因暴露组

Application of spectral analysis to heart rate data collected from infants with intrauterine exposure to cocaine and normal controls showed a significant sleep state effect on HRV, with greater high frequency power seen during quiet sleep (QS) compared to active sleep (AS) and greater low- and mid-frequency power seen in AS compared to QS. However, in both sleep states, the cocaine-exposed neonates showed enhanced total spectral power that appears to be due to an increase in spectral power across all frequency bands. Absolute values for spectral power in the low- and mid-frequency bands of HRV were significantly higher in the cocaine-exposed group in both sleep states. The absolute value for high frequency power was also higher, but this increase attained statistical significance only in quiet sleep. We found no evidence for respiratory patterning differences between the two groups that might account for these findings. Very little of the total respiratory variability in QS and AS was in the low-to-mid-frequency range, suggesting that periodic breathing contributed little to HRV in that same frequency range. We also computed the fractional distribution of heart rate variation across all frequencies as a means of examining sympathovagal balance. Ratios between low- and mid-frequency power compared to high frequency power showed no differences between the groups, although there was a highly significant increase in AS compared to QS. The present results suggest two possibilities: (1) an increase in parasympathetic control of heart rate in the cocaine-exposed infants; or (2) an increase in both vagal and sympathetic modulation of heart rate in the cocaine-exposed group.