Effect of normal and reversed sleep-wake cycles upon nyctohemeral rhythmicity of plasma thyrotropin: evidence suggestive of an inhibitory influence in sleep.
Effect of normal and reversed sleep-wake cycles upon nyctohemeral rhythmicity of plasma thyrotropin: evidence suggestive of an inhibitory influence in sleep.
复制标题
正常和反向睡眠-觉醒周期对血浆促甲状腺素夜间节律的影响：表明睡眠有抑制影响的证据。
DOI：
10.1210/jcem-43-2-318
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
J. Hershman
中科院分区：
文献类型：
--
作者：
D. Parker;A. Pekary;J. Hershman
本文对10名正常青年男子进行了24、36或48小时睡眠监测，每20分钟取血一次，观察血浆TSH昼夜变化与睡眠-觉醒周期的关系。正常睡眠觉醒周期的研究中，睡眠是允许从通常的就寝时间0630小时共21个晚上（晚上= 1840-0620小时）和相应的16天。TSH测定采用放射免疫法。在17个晚上，平均夜间TSH显着超过了一天的，并在18个晚上，在2100-0100小时的时间间隔内，在TSH的明确nytohemerally最大峰值。更大的振幅，持续时间和节奏重复几个晚上区分2100-0100小时最大值持续短暂的情景释放的背景。这些昼夜高峰是睡眠前的最大值，因为上升均匀开始，并在15个晚上，高峰发生在睡眠开始之前。峰值聚集在进入睡眠之前（12个晚上）或之后（3个晚上）的30分钟内。TSH的释放在睡眠中下降。其他证据表明，睡眠对促甲状腺激素释放的抑制作用是，睡眠开始早，在3个晚上没有明确的2100-0100小时促甲状腺激素最大值，平均2100-0100小时促甲状腺激素峰值显着减少时，睡眠开始之前，通常的2300-0000小时的间隔，显着增加时，睡眠开始延迟或推迟。在24小时基线后，4名男性经历了48小时的睡眠-觉醒周期的相位逆转，其中睡眠被转移到1100-1830小时的间隔。在逆转的第一个清醒的夜晚，2100-0100 h的峰值正常开始，但是，在没有睡眠的情况下，增强的TSH释放然后简单地持续整个晚上，延迟夜间最大值的实现。在第二个清醒夜，TSH峰值出现在与第一个清醒夜相同的0400-0600 h，而2100-0100 h的峰值不再明显。TSH的第二个24小时的逆转也显着减少，提示的负反馈效应的增强释放的第一个逆转的一天。在逆转过程中，未观察到基础睡眠前TSH峰值向0900-1300 h间隔或睡眠增强TSH释放的偏移。因此，尽管持续的TSH的昼夜节律性在急性睡眠-觉醒逆转，其模式发生了显着变化，在睡眠中的变化。目前，我们认为这些结果与TSH的昼夜节律性的昼夜节律机制，其表达受到反馈和睡眠的抑制性影响调制的起源是一致的。
The relation of nyctohemeral variation in plasma TSH to sleep-wake cycles was examined in 10 normal young men who had their sleep polygraphically monitored and their blood sampled every 20 min for 24,36, or 48 h periods. Studies of normal sleepwake cycles in which sleep was allowed from the usual bedtime to 0630 h totalled 21 nights (night = 1840-0620 h) and their corresponding 16 days. TSH was measured by a sensitive RIA. On 17 nights, the mean nightly TSH significantly exceeded that of the day's and, on 18 nights, clear nyctohemerally maximal peaks in TSH were seen in the 2100-0100 h interval. Greater amplitude, duration and rhythmic repetition over several nights distinguished 2100-0100 h maxima from a background of persistent briefly episodic release. These nyctohemeral peaks were pre-sleep maxima, as rises uniformly began, and on 15 nights, the peaks occurred prior to the onset of sleep. The peaks clustered within the 30 min just before (12 nights) or after (3 nights) entry into sleep. TSH release then declined across sleep. Other evidence suggestive of an inhibitory influence in sleep upon TSH release was that sleep began early on the 3 nights without clear 2100-0100 h TSH maxima and that the mean 2100-0100 h TSH peak was significantly reduced when sleep began prior to the usual 2300-0000 h interval and significantly increased when the onset of sleep was delayed or postponed. After a 24 h baseline, 4 men underwent phase-reversal of their sleep-wake cycles for 48 h, in which sleep was shifted to the 1100-1830 h interval. On the first wakeful night of reversal, the 2100-0100 h peak began normally, but, in the absence of sleep, the enhanced TSH release then simply continued across this night, delaying achievement of the nyctohemeral maxima. On the second wakeful night of reversal, the maximum in mean TSH lay in the same 0400-0600 h interval as that of first reversal night, and the mean 2100-0100 h peak was no longer evident. The TSH of the second 24 h of reversal also was significantly reduced, suggestive of a negative feedback effect of enhanced release of the first reversal day. No shift of basal pre-sleep TSH peaks to the 0900-1300 h interval or of sleep-enhanced TSH release was seen during reversal. Thus, despite the persistence of TSH's nyctohemeral rhythmicity across acute sleep-wake reversal, its pattern changed significantly in relation to shifts in sleep. We currently view these results as consistent with the origin of TSH's nyctohemeral rhythmicity in a circadian mechanism whose expression is subject to modulation by the inhibitory influences of feedback and sleep.