Document Detail


Sepsis alters vessel contraction by adrenoceptor-induced nitric oxide and prostanoid.
MedLine Citation:
PMID:  12788665     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Alpha-adrenergic agents contract vascular smooth muscle (VSM) and stimulate endothelial release of secondary factors which modulate VSM contraction. Our study examined constrictor prostanoid (cPN) and nitric oxide (NO) as secondary factors which could alter alpha-1 adrenoceptor-mediated contraction during sepsis. METHODS: Sepsis was induced in rats by inoculation of an implanted sponge with Escherichia coli and Bacteroides fragilis. Aortic rings at 24 h from septic (n = 21) and control (n = 21) rats were suspended in physiological salt solution (PSS) with or without blockers to NO (N(G)-monomethylarginine), cPN (mefenamic acid, MFA), or thromboxane A2 (SQ29548). Contraction dose-response curves were generated to determine maximal contraction force (F(max)) and pD2 (sensitivity) to phenylephrine in each experimental group. RESULTS: Sepsis increased F(max) to phenylephrine (PHE) (1.18 vs 0.90 g, SEM 0.0703). COX inhibition reduced the F(max) in control (0.63 vs 0.90 g, SEM 0.0675) but not in septic animals (1.19 vs 1.18 g, SEM 0.0433). TXA2 receptor inhibition did not alter F(max) in control (1.017 vs 0.973 g, SEM 0.0959) or septic animals (1.28 vs 1.12 g, SEM 0.0823). NOS inhibition enhanced the F(max) in both nonseptic (2.03 vs 0.83 g, SEM 0.0523) and septic rats (1.96 vs 1.15 g, SEM 0.0526), but did less so in the septic animals. CONCLUSIONS: PHE-induced F(max) is determined by a balance between PHE-stimulated VSM alpha-adrenoceptor activity, and PHE-stimulated endothelial release of cPN and NO. Sepsis enhances total PHE-induced F(max) by increasing VSM alpha-adrenoceptor activity and reducing PHE-stimulated endothelial release of dilator NO. Sepsis abolishes the PHE-stimulated endothelial release of cPN. PHE-stimulated cPN is not thromboxane A2, but could be a nonprostanoid dilator in the lipoxygenase (HETE) or cytochrome P450 (EET) pathways.
Authors:
Touichi Kawabe; Patrick D Harris; E L Rasheid Zakaria; R Neal Garrison
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The Journal of surgical research     Volume:  110     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  2003 Apr 
Date Detail:
Created Date:  2003-06-05     Completed Date:  2003-07-08     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  352-9     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, School of Medicine HSC-1115, University of Louisville, Louisville, KY 40292, USA. tksmile@bellsouth.net
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta / metabolism,  physiopathology
Bacteroides Infections / metabolism,  physiopathology
Cyclooxygenase Inhibitors / pharmacology
Enzyme Inhibitors / pharmacology
Escherichia coli Infections / metabolism,  physiopathology
Male
Models, Animal
Muscle, Smooth, Vascular / metabolism,  physiopathology*
Nitric Oxide / antagonists & inhibitors,  metabolism*
Nitric Oxide Synthase / antagonists & inhibitors
Phenylephrine / pharmacology
Prostaglandin Antagonists / metabolism
Prostaglandins / metabolism*
Rats
Rats, Sprague-Dawley
Receptors, Adrenergic, alpha-1 / metabolism*
Sepsis / metabolism,  physiopathology*
Thromboxane A2 / antagonists & inhibitors,  metabolism
Vasoconstrictor Agents / metabolism,  pharmacology
Vasodilation / physiology*
Vasodilator Agents / antagonists & inhibitors,  pharmacology
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Enzyme Inhibitors; 0/Prostaglandin Antagonists; 0/Prostaglandins; 0/Receptors, Adrenergic, alpha-1; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 57576-52-0/Thromboxane A2; 59-42-7/Phenylephrine; EC 1.14.13.39/Nitric Oxide Synthase

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