Linked Life Data

11855741

Source:http://linkedlifedata.com/resource/pubmed/id/11855741

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2002-2-21
pubmed:abstractText
In this study we tested the hypothesis that induction of heat shock proteins (HSPs) and antioxidant enzymes is a compensatory mechanism, which preserves the contractility of the surviving myocardium after acute myocardial infarction. For this purpose, mechanical function of isolated rat papillary muscles was tested 15 h after experimental myocardial infarction and sham operation, respectively. Contractility of the preparations was compared to the expression of HSP25, HSP72, and glutathione peroxidase activity (GSH-Px) at normoxia and during hypoxia/reoxygenation. At normoxic conditions, rates of isometric contraction and, in particular, of relaxation were significantly higher after acute myocardial infarction than after sham operation. Improved relaxation rates were reflected in 2- to 3-fold higher heat shock protein levels in papillary muscles from rats with myocardial infarction compared to sham operated animals. During hypoxia/reoxygenation, the rates of contraction and relaxation were better preserved after myocardial infarction than after sham surgery. Recovery of relaxation rates during reoxygenation was associated with increased HSP25 levels and enhanced GSH-Px activity after myocardial infarction. In conclusion, heat shock proteins exert a beneficial effect on cardiac muscle relaxation after acute myocardial infarction. Enhanced heat shock protein expression and GSH-Px activity may protect the contractile function of the surviving myocardium against the damaging influence of hypoxia/reoxygenation during the early post-infarct period.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
228
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
49-55
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11855741-Animals, pubmed-meshheading:11855741-Calcium, pubmed-meshheading:11855741-Cardiomegaly, pubmed-meshheading:11855741-Chronic Disease, pubmed-meshheading:11855741-Creatine Kinase, pubmed-meshheading:11855741-Glutathione Peroxidase, pubmed-meshheading:11855741-HSP27 Heat-Shock Proteins, pubmed-meshheading:11855741-HSP72 Heat-Shock Proteins, pubmed-meshheading:11855741-Heat-Shock Proteins, pubmed-meshheading:11855741-Immunoblotting, pubmed-meshheading:11855741-Male, pubmed-meshheading:11855741-Myocardial Contraction, pubmed-meshheading:11855741-Myocardial Infarction, pubmed-meshheading:11855741-Myocardial Reperfusion Injury, pubmed-meshheading:11855741-Neoplasm Proteins, pubmed-meshheading:11855741-Oxygen, pubmed-meshheading:11855741-Papillary Muscles, pubmed-meshheading:11855741-Rats, pubmed-meshheading:11855741-Rats, Wistar, pubmed-meshheading:11855741-Superoxide Dismutase, pubmed-meshheading:11855741-Ventricular Function, Left
pubmed:year
2001
pubmed:articleTitle
Contractile function of rat myocardium is less susceptible to hypoxia/reoxygenation after acute infarction.
pubmed:affiliation
Institute of Physiology, Humboldt-University, Charité, Berlin, Germany. kay-dietrich.wagner@charite.de
pubmed:publicationType
Journal Article, Comparative Study