Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1994-5-17
|
| pubmed:abstractText |
The role of E-selectin in the pathogenesis of an experimental model of myocardial ischemia-reperfusion injury was investigated. Pentobarbital anesthetized rats underwent left main coronary artery ligation (1 h) followed by reperfusion (1 h; MI/R). Sham operated rats were used as controls (sham MI/R). Myocardial ischemia-reperfusion injury reduced survival rate (50%), caused severe myocardial damage (necrotic area/area-at-risk 69.8 +/- 5%; necrotic area/total area = 56 +/- 7.6%), increased serum creatine phosphokinase activity (sham MI/R = 33 +/- 3 U/ml; MI/R = 215 +/- 13 U/ml), and elevated myeloperoxidase activity (investigated as an index of leukocyte adhesion and accumulation; sham MI/R = 0.11 +/- 0.02 U x 10(-3)/g tissue) in the area-at-risk (7.5 +/- 1.7 U x 10(-3)/g tissue) and in the necrotic area (7.8 +/- 2.2 U x 10(-3)/g tissue). Furthermore, MI/R rats had an increased pressure rate index, studied as a quantitative means for assessing myocardial oxygen demand. Administration of a hyperimmune serum containing antibodies against E-selectin significantly improved survival rate (80%), reduced myocardial injury (necrotic area/area-at-risk = 26.4 +/- 7%, P < 0.005; necrotic area/total area 19.1 +/- 2.8%, P < 0.005), lowered serum creatine phospokinase activity (85 +/- 5 U/ml, P < 0.001) and decreased myeloperoxidase activity in the area at risk (3.7 +/- 1.3 U x 10(-3)/g tissue, P < 0.001) and in the necrotic area (3.0 +/- 0.7 U x 10(-3)/g tissue). Finally, the administration of anti E-selectin antibodies improved the PRI in MI/R rats. The present data suggest that E-selectin in vivo plays a key role in the pathogenesis of myocardial ischemia/reperfusion injury.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Creatine Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidase,
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 |
3
|
| pubmed:volume |
270
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
45-51
|
| pubmed:dateRevised |
2007-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:7512508-Animals,
pubmed-meshheading:7512508-Cell Adhesion Molecules,
pubmed-meshheading:7512508-Creatine Kinase,
pubmed-meshheading:7512508-E-Selectin,
pubmed-meshheading:7512508-Hemodynamics,
pubmed-meshheading:7512508-Immunization, Passive,
pubmed-meshheading:7512508-Male,
pubmed-meshheading:7512508-Myocardial Reperfusion Injury,
pubmed-meshheading:7512508-Peroxidase,
pubmed-meshheading:7512508-Rats,
pubmed-meshheading:7512508-Rats, Sprague-Dawley,
pubmed-meshheading:7512508-Tumor Necrosis Factor-alpha
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
E-selectin in the pathogenesis of experimental myocardial ischemia-reperfusion injury.
|
| pubmed:affiliation |
Institute of Pharmacology, School of Medicine, University of Messina, Italy.
|
| pubmed:publicationType |
Journal Article
|