Document Detail


Acute negative inotropic effects of homocysteine are mediated via the endothelium.
MedLine Citation:
PMID:  15072957     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies have shown that chronic hyperhomocysteinemia is associated with an adverse cardiac remodeling and heart failure. This study, which utilized coronary-perfused hearts and superfused papillary muscle, was designed to determine whether homocysteine acts acutely to alter cardiac contractile function. Left ventricular developed pressure was used as a measure of systolic function in the Langendorff-perfused heart, whereas isometric developed tension was used in papillary muscle. All preparations were bathed in physiological buffer and paced electrically. Initial results showed that homocysteine elicits a relatively rapid onset (maximum effect observed within 5 min), concentration-dependent (10-300 microM), and moderate negative inotropic action (maximum decrease in tension was approximately 15% of control values) in Langendorff-perfused hearts but not in papillary muscle. In contrast, effluent from homocysteine-treated hearts decreased contractility in papillary muscle, and all inotropic actions were largely eliminated when brief Triton X-100 treatment was utilized to inactivate the coronary endothelium in the intact heart. The homocysteine-induced decrease in contractile function was not antagonized by N(omega)-nitro-l-arginine, a nitric oxide synthase inhibitor, or the cyclooxygenase inhibitor indomethacin. Thus data suggest that pathophysiological concentrations of homocysteine elicit an acute negative inotropic effect on ventricular myocardium that is mediated by a coronary endothelium-derived agent other than nitric oxide or products of cyclooxygenase. Future studies are required to elucidate the mechanism by which homocysteine acts to elicit the release of the proposed endothelial mediator, the identity of the proposed paracrine agent, and the mechanism of its negative inotropic action.
Authors:
Richard H Kennedy; Richard Owings; Nawal Shekhawat; Jacob Joseph
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-04-08
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  287     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2004 Aug 
Date Detail:
Created Date:  2004-07-27     Completed Date:  2004-09-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H812-7     Citation Subset:  IM    
Affiliation:
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. kennedyrichardh@uams.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiovascular Agents / pharmacology
Coronary Vessels / physiology*
Drug Synergism
Endothelium, Vascular / physiology*
Enzyme Inhibitors
Heart / drug effects*
Homocysteine / pharmacology*
Indomethacin / pharmacology
Male
Myocardial Contraction / drug effects*,  physiology*
Nitroarginine
Octoxynol / pharmacology
Papillary Muscles / drug effects,  physiology
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Cardiovascular Agents; 0/Enzyme Inhibitors; 2149-70-4/Nitroarginine; 454-28-4/Homocysteine; 53-86-1/Indomethacin; 9002-93-1/Octoxynol

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


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