Document Detail

Transient focal ischemia increases endothelial nitric oxide synthase in cerebral blood vessels.
MedLine Citation:
PMID:  12411665     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND PURPOSE: Production of NO by endothelial NO synthase (eNOS) plays a protective role in cerebral ischemia. We studied the effects of transient focal ischemia on eNOS expression. METHODS: Wistar rats (n=72) underwent reversible filament occlusion of the right middle cerebral artery for 75 minutes. After 6, 24, 72, or 168 hours of reperfusion, brains were removed and coronal sections cut for eNOS immunohistochemistry, eNOS-alkaline phosphatase costaining, and hematoxylin-eosin staining. Samples for eNOS immunoblots were taken from corresponding striatum and overlying parietal cortex bilaterally. RESULTS: eNOS protein occurred in virtually all blood vessels and was consistently increased in microvessels in the ischemic striatum after 24 to 168 hours of reperfusion but not at 6 hours. eNOS upregulation in the parietal cortex was only present in animals with evidence of cortical infarcts documented on adjacent HE-stained sections. Costaining of endogenous alkaline phosphatase and eNOS demonstrated eNOS expression in all segments of cerebral microvessels. Quantitative analysis of eNOS immunostaining and immunoblots showed no attenuated increase in animals that were treated with indomethacin (5 mg/kg IP), NS398 (20 mg/kg IP), or L-arginine-methyl ester (10 mg/kg IP). In contrast to eNOS, levels of brain NOS did not increase after ischemia. CONCLUSION: eNOS protein is upregulated in pre- and postcapillary microvessels and upregulation appears slower after transient compared with permanent ischemia. Cyclooxygenase and NOS products do not play a major role in postischemic eNOS induction.
Roland Veltkamp; Nishadi Rajapakse; Greg Robins; Michelle Puskar; Katsuyoshi Shimizu; David Busija
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Stroke; a journal of cerebral circulation     Volume:  33     ISSN:  1524-4628     ISO Abbreviation:  Stroke     Publication Date:  2002 Nov 
Date Detail:
Created Date:  2002-11-04     Completed Date:  2002-11-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0235266     Medline TA:  Stroke     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2704-10     Citation Subset:  IM    
Department of Physiology and Pharmacology and Center for Investigative Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
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MeSH Terms
Blood Vessels / drug effects,  enzymology*,  pathology
Blotting, Western
Brain / blood supply,  enzymology*,  pathology
Cerebrovascular Circulation*
Corpus Striatum / blood supply,  enzymology,  pathology
Enzyme Inhibitors / pharmacology
Infarction, Middle Cerebral Artery / complications,  enzymology,  pathology
Ischemic Attack, Transient / enzymology*,  etiology,  pathology
Microcirculation / drug effects,  enzymology,  pathology
Nitric Oxide Synthase / antagonists & inhibitors,  metabolism*
Nitric Oxide Synthase Type I
Nitric Oxide Synthase Type III
Parietal Lobe / blood supply,  enzymology,  pathology
Rats, Wistar
Grant Support
Reg. No./Substance:
0/Enzyme Inhibitors; EC Oxide Synthase; EC Oxide Synthase Type I; EC Oxide Synthase Type III; EC protein, rat; EC protein, rat

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