Document Detail


Endomyocardial nitric oxide synthase and left ventricular preload reserve in dilated cardiomyopathy.
MedLine Citation:
PMID:  10368118     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Patients with heart failure have modified myocardial expression of nitric oxide synthase (NOS), as is evident from induction of calcium-insensitive NOS isoforms. The functional significance of this modified NOS gene expression for left ventricular (LV) contractile performance was investigated in patients with dilated nonischemic cardiomyopathy.
METHODS AND RESULTS: In patients with dilated, nonischemic cardiomyopathy, invasive measures of LV contractile performance were derived from LV microtip pressure recordings and angiograms and correlated with intensity of gene expression of inducible (NOS2) and constitutive (NOS3) NOS isoforms in simultaneously procured LV endomyocardial biopsies (n=20). LV endomyocardial expression of NOS2 was linearly correlated with LV stroke volume (P=0.001; r=0.66), LV ejection fraction (P=0.007; r=0.58), and LV stroke work (P=0.003; r=0.62). In patients with elevated LV end-diastolic pressure (>16 mm Hg), a closer correlation was observed between endomyocardial expression of NOS2 and LV stroke volume (P=0.001; r=0.74), LV ejection fraction (P=0.0007; r=0.77), and LV stroke work (r=0.82; P=0.0002). LV endomyocardial expression of NOS3 was linearly correlated with LV stroke volume (P=0.01; r=0.53) and LV stroke work (P=0.01; r=0.52). To establish the role of nitric oxide (NO) as a mediator of the observed correlations, substance P (which causes endothelial release of NO) was infused intracoronarily (n=12). In patients with elevated LV end-diastolic pressure, an intracoronary infusion of substance P increased LV stroke volume from 72+/-13 to 91+/-16 mL (P=0.06) and LV stroke work from 67+/-11 to 90+/-15 g. m (P=0.03) and shifted the LV end-diastolic pressure-volume relation to the right.
CONCLUSIONS: In patients with dilated cardiomyopathy, an increase in endomyocardial NOS2 or NOS3 gene expression augments LV stroke volume and LV stroke work because of a NO-mediated rightward shift of the diastolic LV pressure-volume relation and a concomitant increase in LV preload reserve.
Authors:
C Heymes; M Vanderheyden; J G Bronzwaer; A M Shah; W J Paulus
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Circulation     Volume:  99     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  1999 Jun 
Date Detail:
Created Date:  1999-07-12     Completed Date:  1999-07-12     Revised Date:  2011-10-27    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  3009-16     Citation Subset:  AIM; IM    
Affiliation:
Cardiovascular Center, O.L.V. Ziekenhuis, Aalst, Belgium.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Cardiomyopathy, Dilated / complications,  enzymology,  physiopathology*
Coronary Angiography
Female
Gene Expression Regulation, Enzymologic*
Heart Catheterization
Heart Failure / enzymology,  etiology,  physiopathology*
Humans
Male
Middle Aged
Myocardium / enzymology*
Nitric Oxide Synthase / genetics*,  metabolism
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Regression Analysis
Reverse Transcriptase Polymerase Chain Reaction
Stroke Volume / drug effects
Substance P / pharmacology
Ventricular Function, Left* / drug effects
Chemical
Reg. No./Substance:
33507-63-0/Substance P; EC 1.14.13.39/NOS2 protein, human; EC 1.14.13.39/NOS3 protein, human; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III
Comments/Corrections
Comment In:
Circulation. 1999 Jun 15;99(23):2972-5   [PMID:  10368111 ]

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