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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1994-4-6
|
| pubmed:abstractText |
To determine whether cardiac failure produced by chronic coronary artery stenosis was associated with the activation of myocyte cellular hyperplasia in the myocardium, the changes in number and size of left ventricular myocytes were measured in rats 3 months after surgery. The hypertrophied left ventricle was found to possess 44%, 32%, 49%, and 48% fewer mononucleated, binucleated, trinucleated, and tetranucleated myocytes, respectively. In contrast, the hypertrophied right ventricle contained 1.49 x 10(6) more myocytes as a result of a 2.1-fold, 1.4-fold, and 1.4-fold increase in mononucleated, binucleated, and tetranucleated myocytes. Myocyte cell volume was seen to increase 49% and 21% in left and right ventricular myocytes, respectively. The process of myocyte cellular hyperplasia in the right ventricular myocardium was accompanied by capillary proliferation, and these events were responsible for the parallel addition of newly formed cells and capillaries within the wall and mural thickening. Moreover, the in-series insertion of new myocytes contributed to right ventricular dilatation after coronary artery stenosis. In view of the fact that extensive myocardial damage and cell loss may have masked the phenomenon of myocyte cellular hyperplasia in the left ventricle, the presence of DNA synthesis in myocyte nuclei was evaluated at 3 days, 1 week, 2 weeks, 1 month, and 3 months after coronary artery stenosis. Bromodeoxyuridine (BrdU) labeling markedly increased in myocyte nuclei of both ventricles, reaching its peak at 1 and 2 weeks. BrdU labeling of nonmyocyte nuclei also increased but mostly at 2 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0009-7330
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
74
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
383-400
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:8118947-Animals,
pubmed-meshheading:8118947-Cardiomegaly,
pubmed-meshheading:8118947-Cardiomyopathies,
pubmed-meshheading:8118947-Cell Nucleus,
pubmed-meshheading:8118947-Coronary Vessels,
pubmed-meshheading:8118947-DNA,
pubmed-meshheading:8118947-Heart,
pubmed-meshheading:8118947-Heart Ventricles,
pubmed-meshheading:8118947-Hyperplasia,
pubmed-meshheading:8118947-Hypertrophy,
pubmed-meshheading:8118947-Male,
pubmed-meshheading:8118947-Mitosis,
pubmed-meshheading:8118947-Myocardial Ischemia,
pubmed-meshheading:8118947-Myocardium,
pubmed-meshheading:8118947-Ploidies,
pubmed-meshheading:8118947-Rats,
pubmed-meshheading:8118947-Rats, Sprague-Dawley,
pubmed-meshheading:8118947-Time Factors,
pubmed-meshheading:8118947-Ventricular Function
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
Myocyte cellular hyperplasia and myocyte cellular hypertrophy contribute to chronic ventricular remodeling in coronary artery narrowing-induced cardiomyopathy in rats.
|
| pubmed:affiliation |
Department of Medicine, New York Medical College, Valhalla 10595.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|