Influence of endotoxin on nocturnal sleep in humans.

Standard

Influence of endotoxin on nocturnal sleep in humans. / Pollmächer, T; Schreiber, W; Gudewill, S; Vedder, H; Fassbender, K; Wiedemann, Klaus; Trachsel, L; Galanos, C; Holsboer, F.

in: AM J PHYSIOL-HEART C, Jahrgang 264(6 Pt 2), 1993, S. 1077-1083.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Pollmächer, T, Schreiber, W, Gudewill, S, Vedder, H, Fassbender, K, Wiedemann, K, Trachsel, L, Galanos, C & Holsboer, F 1993, 'Influence of endotoxin on nocturnal sleep in humans.', AM J PHYSIOL-HEART C, Jg. 264(6 Pt 2), S. 1077-1083. <http://www.ncbi.nlm.nih.gov/pubmed/8391756?dopt=Citation>

APA

Pollmächer, T., Schreiber, W., Gudewill, S., Vedder, H., Fassbender, K., Wiedemann, K., Trachsel, L., Galanos, C., & Holsboer, F. (1993). Influence of endotoxin on nocturnal sleep in humans. AM J PHYSIOL-HEART C, 264(6 Pt 2), 1077-1083. http://www.ncbi.nlm.nih.gov/pubmed/8391756?dopt=Citation

Vancouver

Pollmächer T, Schreiber W, Gudewill S, Vedder H, Fassbender K, Wiedemann K et al. Influence of endotoxin on nocturnal sleep in humans. AM J PHYSIOL-HEART C. 1993;264(6 Pt 2):1077-1083.

Bibtex

@article{0e038120105046e1ac43eebb309ae7a4,
title = "Influence of endotoxin on nocturnal sleep in humans.",
abstract = "Sleepiness is a common complaint during infectious diseases, but the interaction between sleep and host defense mechanisms has been poorly explored in humans. We therefore studied the effect of endotoxin, a major pathophysiological factor in gram-negative bacterial infections, on sleep and on parameters of the primary host response in men. In a single-blind counterbalanced trial, 15 healthy volunteers received either placebo or Salmonella abortus equi endotoxin (0.4 ng/kg body wt) intravenously on two separate occasions. Nocturnal sleep was recorded, and rectal temperature and the plasma levels of tumor necrosis factor-alpha, interleukin-6, adrenocorticotropic hormone, and cortisol were monitored for 12 h. Endotoxin reduced the relative amounts of wakefulness (P <0.05) and rapid-eye-movement (REM) sleep (P <0.05) and increased the relative amount of non-REM sleep (P <0.01). Electroencephalogram delta power during non-REM sleep, as measured by spectral analysis, was not altered by endotoxin. The endotoxin-induced changes in sleep structure were related temporally and quantitatively to the increases in rectal temperature and to the release of cytokines and neurohormones. It is concluded that cytokines and neurohormones mediate the effects of endotoxin upon sleep. The ensuing increase in non-REM sleep may be part of the adaptive host response to bacterial infections in humans.",
author = "T Pollm{\"a}cher and W Schreiber and S Gudewill and H Vedder and K Fassbender and Klaus Wiedemann and L Trachsel and C Galanos and F Holsboer",
year = "1993",
language = "Deutsch",
volume = "264(6 Pt 2)",
pages = "1077--1083",
journal = "AM J PHYSIOL-HEART C",
issn = "0363-6135",
publisher = "American Physiological Society",

}

RIS

TY - JOUR

T1 - Influence of endotoxin on nocturnal sleep in humans.

AU - Pollmächer, T

AU - Schreiber, W

AU - Gudewill, S

AU - Vedder, H

AU - Fassbender, K

AU - Wiedemann, Klaus

AU - Trachsel, L

AU - Galanos, C

AU - Holsboer, F

PY - 1993

Y1 - 1993

N2 - Sleepiness is a common complaint during infectious diseases, but the interaction between sleep and host defense mechanisms has been poorly explored in humans. We therefore studied the effect of endotoxin, a major pathophysiological factor in gram-negative bacterial infections, on sleep and on parameters of the primary host response in men. In a single-blind counterbalanced trial, 15 healthy volunteers received either placebo or Salmonella abortus equi endotoxin (0.4 ng/kg body wt) intravenously on two separate occasions. Nocturnal sleep was recorded, and rectal temperature and the plasma levels of tumor necrosis factor-alpha, interleukin-6, adrenocorticotropic hormone, and cortisol were monitored for 12 h. Endotoxin reduced the relative amounts of wakefulness (P <0.05) and rapid-eye-movement (REM) sleep (P <0.05) and increased the relative amount of non-REM sleep (P <0.01). Electroencephalogram delta power during non-REM sleep, as measured by spectral analysis, was not altered by endotoxin. The endotoxin-induced changes in sleep structure were related temporally and quantitatively to the increases in rectal temperature and to the release of cytokines and neurohormones. It is concluded that cytokines and neurohormones mediate the effects of endotoxin upon sleep. The ensuing increase in non-REM sleep may be part of the adaptive host response to bacterial infections in humans.

AB - Sleepiness is a common complaint during infectious diseases, but the interaction between sleep and host defense mechanisms has been poorly explored in humans. We therefore studied the effect of endotoxin, a major pathophysiological factor in gram-negative bacterial infections, on sleep and on parameters of the primary host response in men. In a single-blind counterbalanced trial, 15 healthy volunteers received either placebo or Salmonella abortus equi endotoxin (0.4 ng/kg body wt) intravenously on two separate occasions. Nocturnal sleep was recorded, and rectal temperature and the plasma levels of tumor necrosis factor-alpha, interleukin-6, adrenocorticotropic hormone, and cortisol were monitored for 12 h. Endotoxin reduced the relative amounts of wakefulness (P <0.05) and rapid-eye-movement (REM) sleep (P <0.05) and increased the relative amount of non-REM sleep (P <0.01). Electroencephalogram delta power during non-REM sleep, as measured by spectral analysis, was not altered by endotoxin. The endotoxin-induced changes in sleep structure were related temporally and quantitatively to the increases in rectal temperature and to the release of cytokines and neurohormones. It is concluded that cytokines and neurohormones mediate the effects of endotoxin upon sleep. The ensuing increase in non-REM sleep may be part of the adaptive host response to bacterial infections in humans.

M3 - SCORING: Zeitschriftenaufsatz

VL - 264(6 Pt 2)

SP - 1077

EP - 1083

JO - AM J PHYSIOL-HEART C

JF - AM J PHYSIOL-HEART C

SN - 0363-6135

ER -