Document Detail

Power output is linearly related to MyHC content in rat skinned myocytes and isolated working hearts.
MedLine Citation:
PMID:  15792987     Owner:  NLM     Status:  MEDLINE    
The amount of work the heart can perform during ejection is governed by the inherent contractile properties of individual myocytes. One way to alter contractile properties is to alter contractile proteins such as myosin heavy chain (MyHC), which is known to demonstrate isoform plasticity in response to disease states. The purpose of this study was to examine myocyte functionality over the complete range of MyHC expression in heart, from 100% alpha-MyHC to 100% beta-MyHC, using euthyroid and hypothyroid rats. Peak power output in skinned cardiac myocytes decreased as a nearly linear function of beta-MyHC expression during maximal (r2 = 0.85, n = 44 myocyte preparations) and submaximal (r2 = 0.82, n = 31 myocyte preparations) Ca2+ activation. To determine whether single myocyte function translated to the level of the whole heart, power output was measured in working heart preparations expressing varied ratios of MyHC. Left ventricular power output of isolated working heart preparations also decreased as a linear function of increasing beta-MyHC expression (r2 = 0.82, n = 34 myocyte preparations). These results demonstrate that power output is highly dependent on MyHC expression in single myocytes, and this translates to the performance of working left ventricles.
F Steven Korte; Todd J Herron; Michael J Rovetto; Kerry S McDonald
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2005-03-25
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  289     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-07-14     Completed Date:  2005-09-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H801-12     Citation Subset:  IM    
Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, USA.
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MeSH Terms
Cytological Techniques
Heart / physiology*
Myocardial Contraction / physiology*
Myocardium / metabolism*
Myocytes, Cardiac / metabolism,  physiology*
Myosin Heavy Chains / metabolism*
Protein Isoforms / metabolism
Rats, Sprague-Dawley
Time Factors
Grant Support
Reg. No./Substance:
0/Myosin Heavy Chains; 0/Protein Isoforms

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