Ogawa Yuriko, Kanbayashi Takashi, Saito Yasushi, Takahashi Yuji, Kitajima Tsuyoshi, Takahashi Kenichi, Hishikawa Yasuo, Shimizu Tetsuo
Department of Neuropsychiatry, Akita University School of Medicine, Akita, Japan.
Sleep. 2003 Dec 15;26(8):986-9. doi: 10.1093/sleep/26.8.986.
Sleep deprivation has a profound effect on cardiovascular regulation through the autonomic nervous system. This study examined the effect of 24-hour total sleep deprivation on muscle sympathetic nerve activity (MSNA), which is a direct measurement of the postganglionic sympathetic efferent innervating the vascular bed in the skeletal muscle and other circulatory structures.
The study was performed on 6 young healthy men. The factors exerting influence on MSNA, such as aging, obesity, body posture, activity, intensity of illumination, and food and beverage consumption were strictly controlled. Burst rate and burst incidence were used as parameters of MSNA. The burst rate, burst incidence, heart rate, and systolic and diastolic blood pressure were measured after total sleep deprivation and control sleep. To perform a linear regression analysis of arterial baroreflex (ABR), the incidence of MSNA bursts corresponding to a given diastolic blood pressure (%MSNA) was examined.
The diastolic blood pressure was significantly higher after total sleep deprivation than after control sleep (66.5 +/- 1.7 vs 57.4 +/- 3.3 mm Hg). The burst rate (9.6 +/- 1.8 vs 13.3 +/- 2.7 bursts/min) and burst incidence (21.6 +/- 4.5 vs 30.3 +/- 8.9 bursts/100 heart beats) of MSNA were significantly lower after total sleep deprivation than after control sleep (P < .05). Analysis of the ABR disclosed a significant linear regressive relation between %MSNA and diastolic blood pressure in every subject after both total sleep deprivation and control sleep. This result implies that the ABR regulates the occurrence of MSNA bursts under different diastolic blood pressure conditions. The threshold (X-axis intercept) of the blood pressure regression line (ie, an indicator of the ABR set point) shifted by 12 +/- 4.3 mm Hg toward a higher blood pressure level after total sleep deprivation (P < .05). The ABR sensitivity, or the slope of the regression line, tended to be less steep after total sleep deprivation than after control sleep, although it was not statistically significant (P = .09).
The diastolic blood pressure increased and both burst rate and burst incidence of MSNA decreased after total sleep deprivation. The results show that resetting of the ABR toward a higher blood pressure level occurred after total sleep deprivation. This ABR resetting probably brings about an increase in arterial blood pressure after total sleep deprivation.
睡眠剥夺通过自主神经系统对心血管调节产生深远影响。本研究检测了24小时完全睡眠剥夺对肌肉交感神经活动（MSNA）的影响，MSNA是对支配骨骼肌血管床及其他循环结构的节后交感传出神经的直接测量。
对6名年轻健康男性进行了该研究。严格控制了对MSNA有影响的因素，如衰老、肥胖、身体姿势、活动、光照强度以及食物和饮料摄入。爆发率和爆发发生率被用作MSNA的参数。在完全睡眠剥夺和对照睡眠后测量爆发率、爆发发生率、心率以及收缩压和舒张压。为了对动脉压力反射（ABR）进行线性回归分析，检测了对应于给定舒张压的MSNA爆发发生率（%MSNA）。
完全睡眠剥夺后的舒张压显著高于对照睡眠后（66.5±1.7对57.4±3.3毫米汞柱）。完全睡眠剥夺后的MSNA爆发率（9.6±1.8对13.3±2.7次/分钟）和爆发发生率（21.6±4.5对30.3±8.9次/100次心跳）显著低于对照睡眠后（P<.05）。对ABR的分析显示，在完全睡眠剥夺和对照睡眠后，每个受试者的%MSNA与舒张压之间均存在显著的线性回归关系。这一结果表明，ABR在不同舒张压条件下调节MSNA爆发的发生。完全睡眠剥夺后，血压回归线的阈值（X轴截距），即ABR设定点的一个指标，向更高血压水平移动了12±4.3毫米汞柱（P<.05）。尽管差异无统计学意义（P=.09），但完全睡眠剥夺后的ABR敏感性，即回归线的斜率，相较于对照睡眠后往往更平缓。
完全睡眠剥夺后舒张压升高，MSNA的爆发率和爆发发生率均降低。结果表明，完全睡眠剥夺后ABR向更高血压水平重置。这种ABR重置可能导致完全睡眠剥夺后动脉血压升高。
