| Transient focal ischemia increases endothelial nitric oxide synthase in cerebral blood vessels. | |
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MedLine Citation:
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PMID: 12411665 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Roland Veltkamp; Nishadi Rajapakse; Greg Robins; Michelle Puskar; Katsuyoshi Shimizu; David Busija |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Stroke; a journal of cerebral circulation Volume: 33 ISSN: 1524-4628 ISO Abbreviation: Stroke Publication Date: 2002 Nov |
Date Detail:
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Created Date: 2002-11-04 Completed Date: 2002-11-15 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0235266 Medline TA: Stroke Country: United States |
Other Details:
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Languages: eng Pagination: 2704-10 Citation Subset: IM |
Affiliation:
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Department of Physiology and Pharmacology and Center for Investigative Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC, USA. roland_veltkamp@med.uni-heidelberg.de |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Vessels / drug effects, enzymology*, pathology Blotting, Western Brain / blood supply, enzymology*, pathology Cerebrovascular Circulation* Corpus Striatum / blood supply, enzymology, pathology Enzyme Inhibitors / pharmacology Immunoblotting Immunohistochemistry Infarction, Middle Cerebral Artery / complications, enzymology, pathology Ischemic Attack, Transient / enzymology*, etiology, pathology Male 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 Rats, Wistar Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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HL-30260/HL/NHLBI NIH HHS; HL-46558/HL/NHLBI NIH HHS; HL-50587/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type I; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos1 protein, rat; EC 1.14.13.39/Nos3 protein, rat |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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