Linked Life Data

2403368

Source:http://linkedlifedata.com/resource/pubmed/id/2403368

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-10-19
pubmed:abstractText
This study was designed to clarify mechanisms responsible for cyclophosphamide-induced cardiotoxicity. Rats were divided into 2 groups: the cyclophosphamide group, which received cyclophosphamide (100 mg/kg) intraperitoneally once a day for 4 consecutive days; and the control group, which remained untreated. In each group, myocardial mitochondrial respiratory function, enzymic activities in the respiratory chain, and ventricular acetylcholine and norepinephrine concentrations were measured. In the cyclophosphamide group, decreases in mitochondrial respiratory function and in enzymic activities in the respiratory chain were observed compared with those of the control group. Administration with cyclophosphamide caused increases in acetylcholine and norepinephrine in the myocardium. As an increase in tissue acetylcholine level is reported to be linked with the genesis of myocardial damage, we conclude that cyclophosphamide-induced cardiotoxicity is closely related to mitochondrial dysfunction and that alterations in the autonomic nervous system might be related to this dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0158-5231
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
289-95
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Role of the autonomic nervous system in cyclophosphamide-induced heart mitochondrial dysfunction in rats.
pubmed:affiliation
Department of Internal Medicine, Faculty of Medicine, University of Nagoya, Japan.
pubmed:publicationType
Journal Article