Document Detail

Endomyocardial nitric oxide synthase and left ventricular preload reserve in dilated cardiomyopathy.
MedLine Citation:
PMID:  10368118     Owner:  NLM     Status:  MEDLINE    
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.
C Heymes; M Vanderheyden; J G Bronzwaer; A M Shah; W J Paulus
Related Documents :
2044548 - Non-invasive assessment of systolic left ventricular function in systemic sclerosis.
2736738 - Nonhomogeneous left ventricular regional shortening during acute right ventricular pres...
10452878 - Pressure volume curves in arrested heterotopic rat heart isografts: role of improved my...
8430868 - Sympathetic stimulation alters left ventricular relaxation and chamber size.
2886198 - Respiratory and vasomotor effects of excitatory amino acid on ventral medullary surface.
25215158 - Techniques of rapid sequence induction and intubation at a university teaching hospital.
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    
Cardiovascular Center, O.L.V. Ziekenhuis, Aalst, Belgium.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cardiomyopathy, Dilated / complications,  enzymology,  physiopathology*
Coronary Angiography
Gene Expression Regulation, Enzymologic*
Heart Catheterization
Heart Failure / enzymology,  etiology,  physiopathology*
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
Reg. No./Substance:
33507-63-0/Substance P; EC protein, human; EC protein, human; EC Oxide Synthase; EC Oxide Synthase Type II; EC Oxide Synthase Type III
Comment In:
Circulation. 1999 Jun 15;99(23):2972-5   [PMID:  10368111 ]

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

Previous Document:  Blood flow dynamics in heart failure.
Next Document:  Angiographic anatomy of the inferior right atrial isthmus in patients with and without history of co...