Recent studies have focused on the role of sleep in the homeostatic regulation of the sympathetic nervous and immune systems, and used experimental sleep deprivation to probe these relationships (Dinges, Douglas, Hamarman, Zaugg, and Kapoor 1995; Irwin, Thompson, Miller, Gillin, and Ziegler 1999; Rogers, Szuba, Staab, Evans, and Dinges 2001). During sleep, sympathetic tone and circulating levels of sympathetic catecholamines decline, whereas sleep deprivation leads to nocturnal increases in norepinephrine (NE) and epinephrine (Dodt, Breckling, Derad, Fehm, and Born 1997; Irwin et al. 1999). Acute sleep loss is also associated with alterations in the expression of cytokines and declination in cellular immune responses (Redwine et al. 2000). For instance, decreased activity of natural killer (NK) cell, an immune cell that is considered to be an important marker of immunological defense against tumors responses, was reported due to acute sleep loss (Shakhar and Ben-Eliyahu 1998).
Patients with primary insomnia or with depression show abnormalities in sleep continuity (Bonnet and Arand 1995; Thase, Simons, and Reynolds 1996), but the relationships between disordered sleep and changes in nocturnal sympathetic catecholamines are not well defined in either of these groups. Insomnia is thought to be associated with chronic sympathetic hyperactivity as evidenced by elevated heart rate, body temperature, sympathetic tone, and whole body metabolic rate. Subjects with primary insomnia show nocturnal elevations of circulating levels of norepinephrine and a reduction in NK activity. It was shown that difficulties with sleep maintenance were associated with increases in nocturnal norepinephrine in the insomniacs and partial night sleep deprivation increased nocturnal levels of norepinephrine and decreased NK cell responses (Irwin, McClintick, Costlow, Fortner, White, and Gillin 1996). The above data implicate sleep continuity in the regulation of the immune and sympathetic nervous systems. Impairments of sleep efficiency correlated with nocturnal elevations of norepinephrine in the insomniacs but not in the depressives or controls. These results indicate that insomnia is associated with nocturnal sympathetic arousal and declines of natural immunity.
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