Document Detail

Endothelium-dependent vasodilator response is augmented in peripheral resistance vessels of patients with vasospastic angina.
MedLine Citation:
PMID:  10702649     Owner:  NLM     Status:  MEDLINE    
Although the mechanism underlying coronary conduit artery spasm in vasospastic angina (VAP) remains unknown, coronary endothelial dysfunction has been suggested as playing an important role. However, it remains unknown whether this endothelium-mediated abnormal vasomotion is uniformly evident irrespective of site of vascular bed or vessel size. Plethysmographic studies were carried out to measure changes in forearm resistance vessel blood flow (FBF) induced by acetylcholine (Ach), sodium nitroprusside, and 10-min occlusion-induced reactive hyperemia in 12 patients with VAP, 14 patients with atherosclerotic (>75% fixed stenosis) coronary artery disease (CAD), and 16 healthy controls. FBF responses induced by the endothelium-dependent vasodilator Ach were significantly augmented in patients with VAP compared to controls, whereas this type of FBF response in patients with CAD was significantly blunted (at the maximum dose: VAP, 24.1 +/- 3.0; controls, 17.2 +/- 1.9; CAD, 12.8 +/- 1.9 ml/min per 100 ml; p < 0.01). However, there were no significant differences in FBF responses during infusion of sodium nitroprusside among the three subject groups. Reactive hyperemic FBF which represents maximum vasodilatory capacity did not differ among the three. To assess the role of nitric oxide in the augmented endothelium-dependent response in VAP, Ach-induced FBF response was determined before and after administration of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine in another VAP group (n = 7). After nitric oxide synthase inhibition, the peak FBF response induced by Ach decreased from 23.3 +/- 3.2 to 14.1 +/- 1.6 ml/min per 100 ml (p < 0.05). In conclusion, the above data suggest that endothelium-dependent vasomotor response to Ach in limb resistance vessels is augmented in patients with vasospastic angina. It seems unlikely that endothelial function is consistently depressed in any area of the vascular bed in this disorder.
M Nakamura; H Yoshida; N Arakawa; K Hiramori
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Publication Detail:
Type:  Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiology     Volume:  92     ISSN:  0008-6312     ISO Abbreviation:  Cardiology     Publication Date:  1999  
Date Detail:
Created Date:  2000-05-23     Completed Date:  2000-05-23     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  1266406     Medline TA:  Cardiology     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  85-92     Citation Subset:  IM    
Copyright Information:
Copyright 2000 S. Karger AG, Basel
Second Department of Internal Medicine, Iwate Medical University, Morioka, Japan.
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MeSH Terms
Acetylcholine / pharmacology
Blood Pressure / drug effects
Coronary Disease / diagnosis,  physiopathology
Coronary Vasospasm / diagnosis,  physiopathology*
Dose-Response Relationship, Drug
Endothelium, Vascular / drug effects,  physiopathology*
Forearm / blood supply
Heart Rate / drug effects
Middle Aged
Nitric Oxide Synthase / antagonists & inhibitors
Nitroprusside / pharmacology
Regional Blood Flow / drug effects,  physiology
Vascular Resistance / drug effects,  physiology*
Vasodilator Agents / pharmacology
omega-N-Methylarginine / pharmacology
Reg. No./Substance:
0/Vasodilator Agents; 15078-28-1/Nitroprusside; 17035-90-4/omega-N-Methylarginine; 51-84-3/Acetylcholine; EC Oxide Synthase

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