Document Detail


Functional alterations after cardiac sodium-calcium exchanger overexpression in heart failure.
MedLine Citation:
PMID:  16603685     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The sodium-calcium exchanger (NCX) is discussed as one of the key proteins involved in heart failure. However, the causal role and the extent to which NCX contributes to contractile dysfunction during heart failure are poorly understood. NCX overexpression was induced by infection with an adenovirus coding for NCX, which coexpressed green fluorescence protein (GFP) (AdNCX) by ex vivo gene transfer to nonfailing and failing rabbit cardiomyocytes. Myocardial gene transfer in rabbits in vivo was achieved by adenoviral delivery via aortic cross-clamping. Peak cell shortening of cardiomyocytes was determined photo-optically. Hemodynamic parameters in vivo were determined by echocardiography (fractional shortening) and tip catheter [maximal first derivative of left ventricular (LV) pressure (dP/dt(max)); maximal negative derivative of LV pressure (-dP/dt(max))]. Peak cell shortening was depressed after NCX gene delivery in isolated nonfailing and in failing cardiomyocytes. In nonfailing rabbits in vivo, basal systolic contractility (fractional shortening and dP/dt(max)) and maximum rate of LV relaxation (-dP/dt(max)) in vivo were largely unaffected after NCX overexpression. However, during heart failure, long-term NCX overexpression over 2 wk significantly improved fractional shortening and dP/dt(max) compared with AdGFP-infected rabbits, both without inotropic stimulation and after beta-adrenergic stimulation with isoproterenol. -dP/dt(max) was also improved after NCX overexpression in the failing rabbits group. These results indicate that short-term effects of NCX overexpression impair contractility of isolated failing and nonfailing rabbit cardiomyocytes. NCX overexpression over 2 wk in vivo does not seem to affect myocardial contractility in nonfailing rabbits. Interestingly, in vivo overexpression of NCX decreased the progression of systolic and diastolic contractile dysfunction and improved beta-adrenoceptor-mediated contractile reserve in heart failure in rabbits in vivo.
Authors:
Götz Münch; Kai Rosport; Christine Baumgartner; Zhongmin Li; Silvia Wagner; Andreas Bültmann; Martin Ungerer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-04-07
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  291     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-07-14     Completed Date:  2006-08-18     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H488-95     Citation Subset:  IM    
Affiliation:
Trigen GmbH, Fraunhoferstr. 9, D-82152 Martinsried, Germany. gmuench@trigen.de
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MeSH Terms
Descriptor/Qualifier:
Adenoviridae / genetics
Animals
Blotting, Western
Cells, Cultured
DNA, Complementary / biosynthesis,  genetics
Dogs
Electrocardiography
Gene Transfer Techniques
Genetic Vectors
Heart Failure / metabolism*,  physiopathology*
Heart Function Tests
Heart Rate / physiology
Hemodynamics / physiology
Myocardial Contraction / physiology
Myocytes, Cardiac / metabolism
Rabbits
Recombinant Proteins / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Sodium-Calcium Exchanger / biosynthesis*
Ventricular Function, Left / physiology
Chemical
Reg. No./Substance:
0/DNA, Complementary; 0/Recombinant Proteins; 0/Sodium-Calcium Exchanger

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


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