Linked Life Data

2526720

Source:http://linkedlifedata.com/resource/pubmed/id/2526720

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1989-9-1
pubmed:abstractText
The etiology of the SAS is unknown. To test whether endogenous opioids could be pathologically active in SAS, markers of opioid systems were measured in the CSF of 15 patients with SAS and in control subjects. Measured by receptor assay, the concentration of so-called fraction 1 opioid was higher in patients with SAS (3.0 +/- 1.5 pmol/ml; mean +/- SD) than in control subjects (1.1 +/- 0.5 pmol/ml) (p less than 0.01), whereas that of fraction 2 opioid was similar in the two groups. Beta-endorphin-like activity, measured by radioimmunoassay, was somewhat lower in patients with SAS (14.0 +/- 2.8 pmol/ml) than in control subjects (21.8 +/- 7.6 pmol/ml) (p less than 0.05). Six months after surgical treatment of the soft palate, new measurements were made in eight patients. Fraction 2 endorphin and beta-endorphin showed no consistent changes. A decrease in the level of fraction 1 from 4.1 +/- 1.5 pmol/ml to 2.3 +/- 1.0 pmol/ml (p less than 0.02) was noted in those six patients showing a successful clinical course. The data support the hypothesis that in SAS the opioid activity is increased.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0012-3692
pubmed:author
pubmed:issnType
Print
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
250-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Increased CSF opioid activity in sleep apnea syndrome. Regression after successful treatment.
pubmed:affiliation
Department of Pulmonary Medicine, Uppsala University, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't