Document Detail


Endotoxin differentially impairs receptor-mediated relaxation in rat isolated pulmonary and thoracic aortic vessels.
MedLine Citation:
PMID:  9820693     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: The purpose of this study was to determine the effect of endotoxin on vasorelaxation in the pulmonary and systemic circulations in response to the following agonists that require generation of cyclic adenosine monophosphate: (1) beta-adrenergic receptor stimulation with isoproterenol; (2) H2 receptor stimulation with dimaprit; and (3) adenylate cyclase stimulation with forskolin. METHODS: Male Sprague-Dawley rats weighing 250 to 350 g were injected with endotoxin (20 mg/kg intraperitoneal) or saline. Six hours later, the cumulative dose response to beta-adrenergic receptor stimulation (isoproterenol), H2 receptor stimulation (dimaprit), and adenylate cyclase stimulation (forskolin) was determined in isolated rat pulmonary artery and thoracic aortic rings preconstricted with phenylephrine. RESULTS: Endotoxin caused significant impairment of relaxation to isoproterenol in the pulmonary artery, but the response in the aorta was not different from the control response. In the pulmonary circulation, endotoxin converted the response to dimaprit from vasorelaxation to vasoconstriction. On the other hand, dimaprit resulted in vasorelaxation in the thoracic aorta after endotoxin; however, the response was impaired compared with the control response. Endotoxin did not affect the dose response to forskolin in either the pulmonary artery or the thoracic aorta. CONCLUSION: From these data, we conclude that endotoxin causes regional specific changes in vascular reactivity. These changes in vascular reactivity result in preserved vasorelaxation in the systemic circulation and impairment of vasorelaxation in the pulmonary circulation in response to endotoxin.
Authors:
R C McIntyre; E J Pulido; B Sheridan; D R Meldrum; D D Bensard; D A Fullerton
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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 Journal of trauma     Volume:  45     ISSN:  0022-5282     ISO Abbreviation:  J Trauma     Publication Date:  1998 Nov 
Date Detail:
Created Date:  1998-11-25     Completed Date:  1998-11-25     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376373     Medline TA:  J Trauma     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  862-7     Citation Subset:  AIM; IM    
Affiliation:
Department of Surgery, University of Colorado Health Sciences Center and The Veterans Affairs Medical Center, Denver 80262, USA. robert.mcintyre@uchsc.edu
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / pharmacology
Animals
Aorta, Thoracic / drug effects*
Blood Circulation / drug effects
Blood Pressure / drug effects
Dimaprit / pharmacology
Dose-Response Relationship, Drug
Endotoxins / pharmacology*
Forskolin / pharmacology
Histamine Agonists / pharmacology
Isoproterenol / pharmacology
Male
Pulmonary Artery / drug effects*
Rats
Rats, Sprague-Dawley
Salmonella typhi*
Vascular Resistance / drug effects
Vasodilation / drug effects*
Grant Support
ID/Acronym/Agency:
R29HL49398/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/Endotoxins; 0/Histamine Agonists; 65119-89-3/Dimaprit; 66428-89-5/Forskolin; 7683-59-2/Isoproterenol

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


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