Document Detail


Correlation of alpha-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in rats.
MedLine Citation:
PMID:  16452123     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have analysed alterations of alpha-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of alpha-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of alpha-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in alpha-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance.
Authors:
Donatella Stilli; Leonardo Bocchi; Roberta Berni; Massimiliano Zaniboni; Francesca Cacciani; Christine Chaponnier; Ezio Musso; Giulio Gabbiani; Sophie Clément
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-02-01
Journal Detail:
Title:  Experimental physiology     Volume:  91     ISSN:  0958-0670     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2006 May 
Date Detail:
Created Date:  2006-05-03     Completed Date:  2006-07-07     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  571-80     Citation Subset:  IM    
Affiliation:
Dipartimento di Biologia Evolutiva e Funzionale-Sezione Fisiologia, Università di Parma, Parco Area delle Scienze 11A, 43100, Parma, Italy. donatella.stilli@unipr.it
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism*
Animals
Blood Pressure*
Cardiomegaly / pathology,  physiopathology*
Extracellular Matrix / metabolism,  pathology
Fibrosis
Heart Rate
Heart Ventricles / pathology*,  physiopathology*
Male
Muscle, Skeletal / metabolism,  pathology
Rats
Rats, Wistar
Severity of Illness Index
Statistics as Topic
Ventricular Dysfunction, Left / pathology,  physiopathology*
Ventricular Fibrillation / pathology,  physiopathology*
Chemical
Reg. No./Substance:
0/Actins

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


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