Document Detail


Coronary artery constriction in rats: necrotic and apoptotic myocyte death.
MedLine Citation:
PMID:  9737484     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The purpose of this study was to determine whether coronary artery narrowing was associated with the activation of necrotic and apoptotic myocyte cell death in the myocardium and whether these 2 forms of cell death were restricted to the left ventricle, or involved the other portions of the heart. Coronary artery narrowing was surgically induced in rats, and the animals were killed from 45 minutes to 12 days after surgery. Myocyte apoptosis was detected by the terminal deoxynucleotidyl transferase assay, confocal microscopy, and deoxyribonucleic acid (DNA) agarose gel electrophoresis. Myocyte necrosis was identified by myosin monoclonal antibody labeling of the cytoplasm. A separate group of animals was treated with trimetazidine in an attempt to interfere with tissue injury. Coronary artery narrowing was characterized by myocyte apoptosis in the left ventricle and interventricular septum, which progressively increased from 45 minutes to 6 days. However, apoptosis was not observed at 12 days. Conversely, myocyte necrosis reached its maximum value at 1 day and was still present at 12 days. This form of cell death affected not only the left ventricular free wall and interventricular septum, but also the right ventricle. Cell necrosis markedly exceeded apoptosis at all intervals. At the peak of cell death, myocyte necrosis was 52-fold and 33-fold higher than apoptosis in the left ventricle and septum. In conclusion, necrotic myocyte cell death is the prevailing form of damage produced by coronary artery narrowing, but apoptotic cell death contributes to the loss of myocytes in the ischemic heart. Trimetazidine treatment attenuated the extent of myocardial damage produced by global ischemia.
Authors:
J Kajstura; Y Liu; A Baldini; B Li; G Olivetti; A Leri; P Anversa
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of cardiology     Volume:  82     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  1998 Sep 
Date Detail:
Created Date:  1998-09-28     Completed Date:  1998-09-28     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  30K-41K     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, New York Medical College, Valhalla 10595, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Coronary Disease / drug therapy,  metabolism,  pathology*
DNA / analysis
DNA Nucleotidylexotransferase / metabolism
Electrophoresis, Agar Gel
Follow-Up Studies
Heart Septum / metabolism,  pathology
Heart Ventricles / metabolism,  pathology
Microscopy, Confocal
Myocardium / metabolism,  pathology*
Myosins / metabolism
Necrosis
Rats
Trimetazidine / pharmacology
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
HL-38132/HL/NHLBI NIH HHS; HL-39902/HL/NHLBI NIH HHS; P0-1-43023//PHS HHS
Chemical
Reg. No./Substance:
0/Vasodilator Agents; 5011-34-7/Trimetazidine; 9007-49-2/DNA; EC 2.7.7.31/DNA Nucleotidylexotransferase; EC 3.6.4.1/Myosins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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