Document Detail


Nitric oxide production is maintained in exercising swine with chronic left ventricular dysfunction.
MedLine Citation:
PMID:  12003829     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Left ventricular (LV) dysfunction caused by myocardial infarction (MI) is accompanied by endothelial dysfunction, most notably a loss of nitric oxide (NO) availability. We tested the hypothesis that endothelial dysfunction contributes to impaired tissue perfusion during increased metabolic demands as produced by exercise, and we determined the contribution of NO to regulation of regional systemic, pulmonary, and coronary vasomotor tone in exercising swine with LV dysfunction produced by a 2- to 3-wk-old MI. LV dysfunction resulted in blunted systemic and coronary vasodilator responses to ATP, whereas the responses to nitroprusside were maintained. Exercise resulted in blunted systemic and pulmonary vasodilator responses in MI that resembled the vasodilator responses in normal (N) swine following blockade of NO synthase with N(omega)-nitro-L-arginine (L-NNA, 20 mg/kg iv). However, L-NNA resulted in similar decreases in systemic (43 +/- 3% in N swine and 49 +/- 4% in MI swine), pulmonary (45 +/- 5% in N swine and 49 +/- 4% in MI swine), and coronary (28 +/- 4% in N and 35 +/- 3% in MI) vascular conductances in N and MI swine under resting conditions; similar effects were observed during treadmill exercise. Selective inhibition of inducible NO synthase with aminoguanidine (20 mg/kg iv) had no effect on vascular tone in MI. These findings indicate that while agonist-induced vasodilation is already blunted early after myocardial infarction, the contribution of endothelial NO synthase-derived NO to regulation of vascular tone under basal conditions and during exercise is maintained.
Authors:
David B Haitsma; Daphne Merkus; Jefrey Vermeulen; Pieter D Verdouw; Dirk J Duncker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  282     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2002 Jun 
Date Detail:
Created Date:  2002-05-10     Completed Date:  2002-06-20     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2198-209     Citation Subset:  IM    
Affiliation:
Experimental Cardiology, Thoraxcenter, Erasmus University, Rotterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / pharmacology
Animals
Coronary Circulation / drug effects
Coronary Vessels / drug effects
Endothelium, Vascular / physiopathology
Enzyme Inhibitors / pharmacology
Guanidines / pharmacology
Lung / blood supply
Myocardial Infarction / complications,  physiopathology
Nitric Oxide / biosynthesis*,  physiology
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type II
Nitroarginine / pharmacology
Nitroprusside / pharmacology
Physical Exertion / physiology*
Reproducibility of Results
Swine
Vasodilation / drug effects
Ventricular Dysfunction, Left / etiology,  physiopathology*
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Guanidines; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 2149-70-4/Nitroarginine; 56-65-5/Adenosine Triphosphate; 79-17-4/pimagedine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II

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


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