Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2-3
|
| pubmed:dateCreated |
1999-3-24
|
| pubmed:abstractText |
The present study was designed to evaluate the effect of cyclosporin A in a rat model of myocardial ischaemia reperfusion injury (MI/R). Anaesthetized rats were subjected to total occlusion (20 min) of the left main coronary artery followed by 5 h reperfusion (MI/R). Sham myocardial ischaemia-reperfusion rats (Sham MI/R) were used as controls. Myocardial necrosis, myocardial myeloperoxidase activity (MPO), serum creatinine phosphokinase activity (CPK), serum tumor necrosis factor (TNF-alpha), cardiac mRNA for TNF-alpha, cardiac intercellular adhesion molecule-1 (ICAM-1) immunostaining and myocardial contractility (left ventricle dP/dtmax) were evaluated. Myocardial ischaemia plus reperfusion in untreated rats produced marked myocardial necrosis, increased serum CPK activity and myeloperoxidase activity (a marker of leukocyte accumulation) both in the area-at-risk and in the necrotic area, reduced myocardial contractility and induced a marked increase in the serum levels of the TNF-alpha. Furthermore increased cardiac mRNA for TNF-alpha was measurable within 10 to 20 min of left main coronary artery occlusion in the area-at-risk and increased levels were generally sustained for 0.5 h. Finally, myocardial ischaemia-reperfusion injury increased ICAM-1 staining in the myocardium. Administration of cyclosporin A (0.25, 0.5 and 1 mg/kg as an i.v. infusion 5 min after coronary artery occlusion) lowered myocardial necrosis and myeloperoxidase activity in the area-at-risk and in the necrotic area, decreased serum CPK activity, increased myocardial contractility, reduced serum levels of TNF-alpha and the cardiac cytokine mRNA levels, and blunted ICAM-1 immunostaining in the injured myocardium. The data suggest that cyclosporin A suppresses leukocyte accumulation and protects against myocardial ischaemia-reperfusion injury.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Creatine Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0014-2999
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
8
|
| pubmed:volume |
364
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
159-68
|
| pubmed:dateRevised |
2007-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:9932719-Animals,
pubmed-meshheading:9932719-Creatine Kinase,
pubmed-meshheading:9932719-Cyclosporine,
pubmed-meshheading:9932719-Disease Models, Animal,
pubmed-meshheading:9932719-Gene Expression,
pubmed-meshheading:9932719-Hemodynamics,
pubmed-meshheading:9932719-Immunohistochemistry,
pubmed-meshheading:9932719-Immunosuppressive Agents,
pubmed-meshheading:9932719-Intercellular Adhesion Molecule-1,
pubmed-meshheading:9932719-Leukocytes,
pubmed-meshheading:9932719-Male,
pubmed-meshheading:9932719-Myocardial Infarction,
pubmed-meshheading:9932719-Myocardial Reperfusion,
pubmed-meshheading:9932719-Myocardial Reperfusion Injury,
pubmed-meshheading:9932719-Myocardium,
pubmed-meshheading:9932719-Peroxidase,
pubmed-meshheading:9932719-RNA, Messenger,
pubmed-meshheading:9932719-Rats,
pubmed-meshheading:9932719-Rats, Sprague-Dawley,
pubmed-meshheading:9932719-Tumor Necrosis Factor-alpha
|
| pubmed:year |
1999
|
| pubmed:articleTitle |
Cyclosporin-A reduces leukocyte accumulation and protects against myocardial ischaemia reperfusion injury in rats.
|
| pubmed:affiliation |
Institute of Pharmacology, School of Medicine, University of Messina, Italy.
|
| pubmed:publicationType |
Journal Article
|