Document Detail


Coronary vascular smooth muscle function in E. coli endotoxemia in dogs.
MedLine Citation:
PMID:  2000978     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The purpose of this study was to determine whether intrinsic contraction-relaxation properties of coronary arteries are altered during acute gram-negative endotoxemia. Coronary vascular smooth muscle (VSM) was evaluated in vitro using large and small left circumflex coronary ring preparations isolated from dogs 4 h after administration of either saline (control; C) or 1.5 mg/kg Escherichia coli endotoxin (ET). ET dogs exhibited marked systemic hypotension and cardiovascular depression throughout the 4-h in vivo phase of the study accompanied by reduction in total left ventricular myocardial blood flow. Isolated coronary vessels were stretched to the apex of the length-contractile tension curve; no differences were observed in length-active or length-passive tension (vessel compliance) relationships between C and ET vessels. Isometric contractions produced by K+ and prostaglandin F2 alpha (PGF2 alpha) were similar in C and ET coronary arteries. VSM relaxant responses to nitroprusside (NP; 10(-10) to 10(-4) M) were also similar in C and ET vessels. In contrast to the apparent lack of effect of ET on directly acting VSM agents, relaxation responses to the endothelial-dependent vasodilator acetylcholine (ACh) were significantly less in ET vessels. Impaired vasodilator response to ACh was not improved by in vivo treatment with the combination antioxidant therapy of allopurinol, superoxide dismutase, and catalase. We conclude that both depolarization (K+) and receptor (PGF2 alpha)-mediated contractile mechanisms, as well as basal cGMP (NP)-mediated vasodilator mechanisms, remained functional in coronary vasculature during acute endotoxemia. Inhibition of ACh-mediated relaxation in ET vessels suggests altered endothelial-dependent vasodilation in coronary arteries during endotoxemia, but this change did not seem to be associated causally with oxygen free radicals.
Authors:
J L Parker; R S Keller; D V DeFily; M H Laughlin; M J Novotny; H R Adams
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  260     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1991 Mar 
Date Detail:
Created Date:  1991-04-11     Completed Date:  1991-04-11     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H832-41     Citation Subset:  IM    
Affiliation:
John M. Dalton Research Center, University of Missouri, Columbia 65211.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Animals
Coronary Vessels / drug effects,  pathology,  physiopathology*
Dinoprost / pharmacology
Dogs
Endotoxins / blood*
Escherichia coli*
Free Radical Scavengers
Male
Muscle, Smooth, Vascular / drug effects,  physiopathology*
Nitroprusside / pharmacology
Potassium Chloride / pharmacology
Vasoconstriction
Vasodilation
Grant Support
ID/Acronym/Agency:
HL-36079/HL/NHLBI NIH HHS; HL-36531/HL/NHLBI NIH HHS; K04-HL-01169/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Endotoxins; 0/Free Radical Scavengers; 15078-28-1/Nitroprusside; 51-84-3/Acetylcholine; 551-11-1/Dinoprost; 7447-40-7/Potassium Chloride

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


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