Document Detail

Endothelial dysfunction in rat mesenteric resistance artery after transient middle cerebral artery occlusion.
MedLine Citation:
PMID:  18258783     Owner:  NLM     Status:  MEDLINE    
Stroke triggers a local and systemic inflammatory response leading to the production of cytokines that can influence blood vessel reactivity. In this study, we aimed to assess whether cerebral ischemia/reperfusion could affect vasoconstriction and vasodilatation on mesenteric resistance arteries (MRA) from Wistar Kyoto rats. The right middle cerebral artery was occluded (90 min) and reperfused (24 h). Sham-operated animals were used as controls. Plasma levels of interleukin (IL)-6 and IL-1beta were measured at 24 h. Vasoconstrictor and vasodilator responses were recorded in a wire myograph. Protein expression was determined by Western blot and immunofluorescence, and superoxide anion (O(2)(.)) production was evaluated by ethidium fluorescence. In MRA, ischemia/reperfusion increased plasma levels of IL-6, O2. production, protein expression of cyclooxygenase-2, and protein tyrosine nitrosylation, but it impaired acetylcholine (ACh) vasodilatation without modifying the vasodilatations to sodium nitroprusside or the contractions to phenylephrine and KCl. Superoxide dismutase (SOD) and indomethacin reversed the impairment of ACh relaxation induced by ischemia/reperfusion. However, N(omega)-nitro-l-arginine methyl ester affected similarly ACh-induced vasodilatations in MRA of ischemic and sham-operated rats. Protein expression of endothelial and inducible nitric-oxide synthase, copper/zinc SOD, manganese SOD, and extracellular SOD was similar in both groups of rats. Our results show MRA endothelial dysfunction 24 h after brain ischemia/reperfusion. Excessive production of O2. in MRA mediates endothelial dysfunction, and the increase in plasma cytokine levels after brain ischemia/reperfusion might be involved in this effect.
Sonia Martinez-Revelles; Francesc Jiménez-Altayó; Laura Caracuel; Fernando J Pérez-Asensio; Anna M Planas; Elisabet Vila
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-02-07
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  325     ISSN:  1521-0103     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-04-18     Completed Date:  2008-05-19     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  363-9     Citation Subset:  IM    
Departament de Farmacologia, Terapèutica i Toxicologia, Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain.
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MeSH Terms
Acetylcholine / pharmacology
Cyclooxygenase 2 / metabolism
Cyclooxygenase Inhibitors / pharmacology
Endothelium, Vascular / drug effects,  physiopathology*
Indomethacin / pharmacology
Infarction, Middle Cerebral Artery / blood,  metabolism,  physiopathology*
Interleukin-1beta / blood*
Interleukin-6 / blood*
Mesenteric Arteries / drug effects,  physiopathology*
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type II / metabolism
Nitric Oxide Synthase Type III
Nitroprusside / pharmacology
Rats, Inbred WKY
Superoxide Dismutase / metabolism,  pharmacology
Superoxides / metabolism*
Vasoconstriction / drug effects
Vasodilator Agents / pharmacology
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Interleukin-1beta; 0/Interleukin-6; 0/Vasodilator Agents; 11062-77-4/Superoxides; 15078-28-1/Nitroprusside; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-84-3/Acetylcholine; 53-86-1/Indomethacin; EC Oxide Synthase; EC Oxide Synthase Type II; EC Oxide Synthase Type III; EC protein, rat; EC protein, rat; EC 2; EC Dismutase

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