Document Detail


Cyclooxygenase-2-dependent superoxide generation contributes to age-dependent impairment of G protein-mediated cerebrovasodilation.
MedLine Citation:
PMID:  12766646     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Previous studies have observed that activation of cyclooxygenase-2 contributes to generation of superoxide anion after fluid percussion brain injury (FPI). This study was designed to characterize the effects of FPI on the vascular activity of two activators of a pertussis toxin-sensitive G protein, mastoparan and mastoparan-7, and the role of cyclooxygenase-2-dependent superoxide anion generation in such effects as a function of age. METHODS: Lateral FPI was induced in anesthetized newborn (1-5-day-old) and juvenile (3-4-week-old) pigs equipped with a closed cranial window. RESULTS: Mastoparan (10(-8), 10(-6) M) elicited pial artery dilation that was blunted more in newborn versus juvenile pigs (9 +/- 1 and 16 +/- 1 vs. 3 +/- 1 and 5 +/- 1%, newborn; 9 +/- 1 and 15 +/- 1 vs. 6 +/- 1 and 9 +/- 1%, juveniles). Similar results were observed for mastoparan-7 but the inactive analog mastoparan-17 had no effect on pial artery diameter. Indomethacin (a cyclooxygenase-1 and cyclooxygenase-2 inhibitor), NS398 (a cyclooxygenase-2 inhibitor), and polyethylene glycol superoxide dismutase and catalase (free radical scavengers) partially restored impaired mastoparan dilation after FPI in the newborn in a roughly equivalent manner but not in the juvenile (3 +/- 1 and 5 +/- 1 vs. 8 +/- 1 and 13 +/- 1% newborn, 6 +/- 1 and 9 +/- 1 vs. 7 +/- 1 and 10 +/- 1% juvenile for NS398 pretreatment). CONCLUSIONS: These data show that G protein activation elicits cerebrovasodilation that is blunted following FPI in an age-dependent manner, and suggest that cyclooxygenase-2-dependent superoxide anion generation contributes to G protein activation-induced dilator impairment after the insult in an age-dependent manner.
Authors:
William M Armstead
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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:  Anesthesiology     Volume:  98     ISSN:  0003-3022     ISO Abbreviation:  Anesthesiology     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-05-26     Completed Date:  2003-06-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  1300217     Medline TA:  Anesthesiology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1378-83     Citation Subset:  AIM; IM    
Affiliation:
Department of Anesthesia, University of Pennsylvania, Philadelphia, 19104, USA. armsteaw@uphs.upenn.edu
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MeSH Terms
Descriptor/Qualifier:
Aging / metabolism*,  physiology
Animals
Animals, Newborn
Arteries / physiology
Blood Chemical Analysis
Brain Injuries / physiopathology
Catalase / pharmacology
Cerebrovascular Circulation / physiology*
Cyclooxygenase 2
Cyclooxygenase 2 Inhibitors
Cyclooxygenase Inhibitors / pharmacology
Female
Free Radical Scavengers / pharmacology
GTP-Binding Proteins / physiology*
Indomethacin / pharmacology
Isoenzymes / metabolism*
Male
Nitrobenzenes / pharmacology
Peptides
Pertussis Toxin / pharmacology
Prostaglandin-Endoperoxide Synthases / metabolism*
Sulfonamides / pharmacology
Superoxide Dismutase / pharmacology
Superoxides / metabolism*
Swine
Vasodilation / physiology*
Wasp Venoms / pharmacology
Chemical
Reg. No./Substance:
0/Cyclooxygenase 2 Inhibitors; 0/Cyclooxygenase Inhibitors; 0/Free Radical Scavengers; 0/Isoenzymes; 0/Nitrobenzenes; 0/Peptides; 0/Sulfonamides; 0/Wasp Venoms; 11062-77-4/Superoxides; 123653-11-2/N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 53-86-1/Indomethacin; 72093-21-1/mastoparan; EC 1.11.1.6/Catalase; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases; EC 1.15.1.1/Superoxide Dismutase; EC 2.4.2.31/Pertussis Toxin; EC 3.6.1.-/GTP-Binding Proteins

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


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