Linked Life Data

7496610

Source:http://linkedlifedata.com/resource/pubmed/id/7496610

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-1-17
pubmed:abstractText
Despite considerable progress in our understanding of the phenomenology of sleep and wakefulness, their regulation and peculiar functions are poorly understood. Recent animal research has revealed considerable evidence for interactions between host defense and sleep. Therefore, it has been hypothesized that host response mediators, mainly cytokines like interleukin-1 (IL-1), are involved in physiological sleep regulation. Furthermore, it has been suggested that sleep, and non rapid eye movement (NREM) sleep in particular, has an immuno-supportive function. In humans, sleep-host defense interactions are just starting to be understood. There is quite good evidence that some viral diseases cause excessive sleepiness. Other infectious diseases induce, however, serious disturbances of the distribution of sleep and wakefulness rather than excessive sleep. In addition, some disorders with excessive sleep, daytime fatigue or disturbed night sleep as prominent symptoms are thought to involve, at least in part, immuno-pathophysiological mechanisms. Experimental settings have only recently been used to elucidate host defense-sleep interactions in humans. The effects of endotoxin, a cell-wall lipopolysaccharide of gram-negative bacteria, on sleep have been tested in different settings in healthy volunteers. Endotoxin transiently suppresses rapid eye movement (REM) sleep independently of the time of the day of administration. Only low doses, given in the evening, promote NREM sleep. Electorencephalogram (EEG) power in higher frequency bands is enhanced during NREM sleep, whereas delta activity is not affected. In rats and rabbits, on the other hand, the effects of endotoxin and of the mediators of its activity on REM sleep are variable. Enhanced NREM sleep is a common finding and most pronounced during the active part of the nycthemeron and, in general, EEG delta activity is augmented. In view of these species differences, hypotheses regarding the underlying mechanisms and the biological significance of host defense-sleep interactions, primarily derived from the results of animal studies, may not entirely fit human physiology. They should therefore be re-evaluated and probably modified, through the use of additional experimental approaches in humans.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0960-5428
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
155-69
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Influence of host defense activation on sleep in humans.
pubmed:affiliation
Max-Planck-Institute of Psychiatry, Clinical Institute, Munich, Germany.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't