Linked Life Data

2839424

Source:http://linkedlifedata.com/resource/pubmed/id/2839424

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1988-8-25
pubmed:abstractText
This study was designed to elucidate the mechanism responsible for alterations in the numbers of autonomic nerve receptors in experimental asthma. In the in vivo experiment, guinea pigs sensitized by exposure to aerosol of 2% ovalbumin for 7-8 min for 10 successive days were used as the experimental asthma group. The control group was exposed to saline. Beta-, alpha-1-adrenergic and muscarinic acetylcholine receptors in lung membranes were studied by direct binding techniques using l-3H-dihydroalprenolol, 3H-bunazosin and l-3H-quinuclidinyl benzilate, respectively. The experimental asthma group showed a 33% decrease in the number of beta-adrenergic receptors, a 37% increase in the number of alpha-1-adrenergic receptors and no change in the number of muscarinic acetylcholine receptors compared with the control group. The endogenous phospholipase activity was determined by high-performance liquid chromatography using tridecanoyl phosphatidylcholine as a substrate. The phospholipase activity in lung membranes in the experimental asthma group was elevated by 50% compared with that in the control group. Lung membrane phospholipid composition was analyzed by thin-layer chromatography with a flame ionization detector. In the experimental asthma group, the amounts of phosphatidylcholine and phosphatidylethanolamine decreased significantly compared with those in the control group. In the in vitro experiment after pretreatment of lung membranes with phospholipase A2, a decreased number of beta-adrenergic receptors, an increased number of alpha-1-adrenergic receptors and no change in the number of muscarinic acetylcholine receptors were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0020-5915
pubmed:author
pubmed:issnType
Print
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
170-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Mechanism responsible for alterations in numbers of autonomic nerve receptors in experimental asthma.
pubmed:affiliation
Department of Internal Medicine, Faculty of Medicine, University of Nagoya, Japan.
pubmed:publicationType
Journal Article