Literature DB >> 3740478

Regional differences in myocyte size in normal rat heart.

A M Gerdes, J A Moore, J M Hines, P A Kirkland, S P Bishop.   

Abstract

Three independent methods were evaluated in an effort to obtain reliable values for myocyte size in adult Sprague-Dawley rats. Cell volume was determined from isolated myocytes by a Coulter Channelyzer system. Cell volume was also determined from the product of length and cross-sectional area of isolated myocytes. Additionally, myocyte cross-sectional area was measured morphometrically from electron micrographs of whole perfusion-fixed tissue. A major goal was to determine if anatomical methods used to measure cell volume produce values comparable to the more expeditious and objective Coulter Channelyzer method. The results of these experiments showed that myocyte dimensions obtained from all three techniques were similar. The second major objective was to use the above-mentioned techniques to evaluate regional differences in myocyte size. Myocyte cross-sectional area and volume were significantly larger in the endomyocardium than in the epimyocardium of the left ventricle. Right ventricle myocytes had significantly smaller volumes and cross-sectional areas than did left ventricle myocytes. There were no regional differences in cell lengths. We conclude that the Coulter Channelyzer system gives values for isolated myocyte volume that are similar to values obtained with histometric techniques; values for isolated myocyte cross-sectional area were representative of values obtained from myocytes in whole-sectioned tissue; significant regional differences in myocyte size are present in adult rat hearts; and regional variations in myocyte size are due to differences in myocyte cross-sectional area rather than cell length.

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Year:  1986        PMID: 3740478     DOI: 10.1002/ar.1092150414

Source DB:  PubMed          Journal:  Anat Rec        ISSN: 0003-276X


  31 in total

1.  Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction.

Authors:  Jiaxiang Qu; Jibin Zhou; Xian Ping Yi; Baojun Dong; Hanqiao Zheng; Lisa M Miller; Xuejun Wang; Michael D Schneider; Faqian Li
Journal:  J Mol Cell Cardiol       Date:  2007-06-21       Impact factor: 5.000

2.  Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

Authors:  K C Chang; V M Figueredo; J H Schreur; K Kariya; M W Weiner; P C Simpson; S A Camacho
Journal:  J Clin Invest       Date:  1997-10-01       Impact factor: 14.808

3.  Stereological estimates of nuclear number in human ventricular cardiomyocytes before and after birth obtained using physical disectors.

Authors:  T M Mayhew; A Pharaoh; A Austin; D G Fagan
Journal:  J Anat       Date:  1997-07       Impact factor: 2.610

Review 4.  Role of thyroid hormones in ventricular remodeling.

Authors:  Viswanathan Rajagopalan; A Martin Gerdes
Journal:  Curr Heart Fail Rep       Date:  2015-04

5.  Myocyte loss in early left ventricular hypertrophy of experimental renovascular hypertension.

Authors:  Moriz Buzello; Christoph Boehm; Stephan Orth; Bernhard Fischer; Heimo Ehmke; Eberhard Ritz; Gerhard Mall; Kerstin Amann
Journal:  Virchows Arch       Date:  2003-04-02       Impact factor: 4.064

6.  Hyperplasia of myocyte nuclei in long-term cardiac hypertrophy in rats.

Authors:  G Olivetti; R Ricci; P Anversa
Journal:  J Clin Invest       Date:  1987-12       Impact factor: 14.808

7.  Novel large-particle FACS purification of adult ventricular myocytes reveals accumulation of myosin and actin disproportionate to cell size and proteome in normal post-weaning development.

Authors:  Javier E López; Janhavi Sharma; Jorge Avila; Taylor S Wood; Jonathan E VanDyke; Bridget McLaughlin; Craig K Abbey; Andrew Wong; Bat-Erdene Myagmar; Philip M Swigart; Paul C Simpson; Nipavan Chiamvimonvat
Journal:  J Mol Cell Cardiol       Date:  2017-08-02       Impact factor: 5.000

8.  Myofibrillar adaptations during cardiac hypertrophy.

Authors:  R L Toffolo; C D Ianuzzo
Journal:  Mol Cell Biochem       Date:  1994-02-23       Impact factor: 3.396

9.  The prevalent I686T human variant and loss-of-function mutations in the cardiomyocyte-specific kinase gene TNNI3K cause adverse contractility and concentric remodeling in mice.

Authors:  Peiheng Gan; Catalin Baicu; Hirofumi Watanabe; Kristy Wang; Ge Tao; Daniel P Judge; Michael R Zile; Takako Makita; Rupak Mukherjee; Henry M Sucov
Journal:  Hum Mol Genet       Date:  2021-01-06       Impact factor: 6.150

10.  Cardiac ultrastructural abnormalities in Syrian hamsters with spontaneous cardiomyopathy or subjected to cardiac overloads.

Authors:  J Perennec; M Willemin; P Pocholle; P Y Hatt; B Crozatier
Journal:  Basic Res Cardiol       Date:  1992 Jan-Feb       Impact factor: 17.165

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