Document Detail


Myosin heavy chain synthesis during the progression of chronic tachycardia induced heart failure in rabbits.
MedLine Citation:
PMID:  9538937     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic tachycardia causes LV dilatation and dysfunction, with no hypertrophy. However, the contributing mechanisms responsible for the left ventricular (LV) remodeling in the absence of myocardial growth in this model of heart failure remain unclear. Therefore, the goal of the present study was to serially examine changes in LV function, steady state myosin heavy chain (MHC) mRNA levels, in vivo synthesis rates, and abundance with the progression of chronic tachycardia induced heart failure. Adult rabbits (3.5-4.5 kg) were studied after one, two, or three weeks of pacing ventricular tachycardia (VT; 400 bpm) and in controls (n = 6 for all groups). LV fractional shortening was reduced by 30% at week one and by over 50% at week three of chronic VT. End-diastolic dimension (EDD) increased at week two compared to controls (1.66 +/- 0.10 vs 1.35 +/- 0.11 cm, p < 0.05) and increased further at week three of VT (1.70 +/- 0.06 cm, p < 0.05). The progressive changes in LV geometry and function with chronic VT were not associated with concomitant time dependent changes in LV mass or MHC mRNA levels. In contrast, MHC fractional synthesis rates increased and reached statistical significance at week three of VT compared to controls (8.3 +/- 0.8 vs 5.5 +/- 0.5%/day, p < 0.05). Despite the stable or increased MHC protein synthesis rates, there was no change in MHC protein abundance at any point during the progression of VT induced heart failure, implicating enhanced MHC protein degradation. Thus, this study demonstrated that a contributory mechanism for the LV remodeling and lack of myocardial growth, which occurs with VT induced heart failure, is enhanced contractile protein degradative processes.
Authors:
D M Eble; J D Walker; A M Samarel; F G Spinale
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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:  Basic research in cardiology     Volume:  93     ISSN:  0300-8428     ISO Abbreviation:  Basic Res. Cardiol.     Publication Date:  1998 Feb 
Date Detail:
Created Date:  1998-05-19     Completed Date:  1998-05-19     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0360342     Medline TA:  Basic Res Cardiol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  50-5     Citation Subset:  IM    
Affiliation:
Cardiovascular Institute, Loyola University Chicago, Maywood, IL 60153, USA. deble@luc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Northern
Cardiac Pacing, Artificial / adverse effects
Chronic Disease
Disease Models, Animal
Disease Progression
Echocardiography
Follow-Up Studies
Heart Failure / etiology,  metabolism*
Myocardium / metabolism*
Myosin Heavy Chains / biosynthesis*,  genetics
RNA, Messenger / metabolism
Rabbits
Tachycardia, Ventricular / complications*,  metabolism
Ventricular Function, Left
Grant Support
ID/Acronym/Agency:
F32HL09611/HL/NHLBI NIH HHS; HL45024/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Myosin Heavy Chains; 0/RNA, Messenger

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


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