Hyperglycemia triggers massive neutrophil deposition in brain following transient ischemia in rats
Myeloperoxidase (MPO) immunohistochemistry was used to ascertain the role of polymorphonuclear leukocytes in hyperglycemia-induced accentuation of brain injury after transient ischemia. Rats received 12.5 min of normothermic global cerebral ischemia by bilateral carotid occlusion plus hypotension. H...
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Veröffentlicht in: | Neuroscience letters 2000-01, Vol.278 (1-2), p.1-4 |
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description | Myeloperoxidase (MPO) immunohistochemistry was used to ascertain the role of polymorphonuclear leukocytes in hyperglycemia-induced accentuation of brain injury after transient ischemia. Rats received 12.5 min of normothermic global cerebral ischemia by bilateral carotid occlusion plus hypotension. Hyperglycemia was induced before ischemia by intraperitoneal dextrose administration. Quantitative MPO immunohistochemistry was performed at 24 h and 3 days postischemia. Brains of normoglycemic-ischemic animals contained almost no MPO activity. By contrast, striking numbers of MPO-positive cells were present in brains studied 24 h after hyperglycemic ischemia, both within pial and parenchymal vessels and within the parenchyma. MPO deposition tended to subside at 3 days. These results indicate that hyperglycemia triggers the early, massive deposition of neutrophils in the postischemic brain--an event that may contribute to exacerbation of injury. |
doi_str_mv | 10.1016/S0304-3940(99)00889-7 |
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Rats received 12.5 min of normothermic global cerebral ischemia by bilateral carotid occlusion plus hypotension. Hyperglycemia was induced before ischemia by intraperitoneal dextrose administration. Quantitative MPO immunohistochemistry was performed at 24 h and 3 days postischemia. Brains of normoglycemic-ischemic animals contained almost no MPO activity. By contrast, striking numbers of MPO-positive cells were present in brains studied 24 h after hyperglycemic ischemia, both within pial and parenchymal vessels and within the parenchyma. MPO deposition tended to subside at 3 days. These results indicate that hyperglycemia triggers the early, massive deposition of neutrophils in the postischemic brain--an event that may contribute to exacerbation of injury.</description><identifier>ISSN: 0304-3940</identifier><identifier>DOI: 10.1016/S0304-3940(99)00889-7</identifier><identifier>PMID: 10643786</identifier><language>eng</language><publisher>Ireland</publisher><subject>Animals ; Blood-Brain Barrier ; Brain - pathology ; Cell Adhesion ; Endothelium, Vascular - pathology ; Glucose - toxicity ; Hyperglycemia - complications ; Hyperglycemia - pathology ; Ischemic Attack, Transient - complications ; Ischemic Attack, Transient - pathology ; Male ; myeloperoxidase ; Neutrophils - pathology ; Peroxidase - analysis ; Rats ; Rats, Wistar ; Reperfusion Injury - etiology ; Reperfusion Injury - pathology</subject><ispartof>Neuroscience letters, 2000-01, Vol.278 (1-2), p.1-4</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10643786$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, B</creatorcontrib><creatorcontrib>Ginsberg, M D</creatorcontrib><creatorcontrib>Busto, R</creatorcontrib><creatorcontrib>Li, L</creatorcontrib><title>Hyperglycemia triggers massive neutrophil deposition in brain following transient ischemia in rats</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Myeloperoxidase (MPO) immunohistochemistry was used to ascertain the role of polymorphonuclear leukocytes in hyperglycemia-induced accentuation of brain injury after transient ischemia. Rats received 12.5 min of normothermic global cerebral ischemia by bilateral carotid occlusion plus hypotension. Hyperglycemia was induced before ischemia by intraperitoneal dextrose administration. Quantitative MPO immunohistochemistry was performed at 24 h and 3 days postischemia. Brains of normoglycemic-ischemic animals contained almost no MPO activity. By contrast, striking numbers of MPO-positive cells were present in brains studied 24 h after hyperglycemic ischemia, both within pial and parenchymal vessels and within the parenchyma. MPO deposition tended to subside at 3 days. These results indicate that hyperglycemia triggers the early, massive deposition of neutrophils in the postischemic brain--an event that may contribute to exacerbation of injury.</description><subject>Animals</subject><subject>Blood-Brain Barrier</subject><subject>Brain - pathology</subject><subject>Cell Adhesion</subject><subject>Endothelium, Vascular - pathology</subject><subject>Glucose - toxicity</subject><subject>Hyperglycemia - complications</subject><subject>Hyperglycemia - pathology</subject><subject>Ischemic Attack, Transient - complications</subject><subject>Ischemic Attack, Transient - pathology</subject><subject>Male</subject><subject>myeloperoxidase</subject><subject>Neutrophils - pathology</subject><subject>Peroxidase - analysis</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - etiology</subject><subject>Reperfusion Injury - pathology</subject><issn>0304-3940</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kEFPxCAQhTlo3HX1J2g4GT1UoUChR7NZXZNNPKjnhqW0i6FQgWr230t09TKTvPfmy8sAcIHRLUa4untBBNGC1BRd1_UNQkLUBT8C8395Bk5jfEcIMczoCZhhVFHCRTUH2_V-1KG3e6UHI2EKpu91iHCQMZpPDZ2eUvDjzljY6tFHk4x30Di4DTLPzlvrv4zr86V00WiXoIlq9wPLfpApnoHjTtqozw97Ad4eVq_LdbF5fnxa3m-KsSQiFaVscck4qVjHOOVtR0tKpGYl05hjltsyJrJAMWeY1EqQmmMhKlURqZRUZAGufrlj8B-TjqkZchVtrXTaT7HBmUox5Tl4eQhO20G3zRjMIMO--fsK-QaqimQ8</recordid><startdate>20000107</startdate><enddate>20000107</enddate><creator>Lin, B</creator><creator>Ginsberg, M D</creator><creator>Busto, R</creator><creator>Li, L</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope></search><sort><creationdate>20000107</creationdate><title>Hyperglycemia triggers massive neutrophil deposition in brain following transient ischemia in rats</title><author>Lin, B ; Ginsberg, M D ; Busto, R ; Li, L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p238t-2ad1257365f5747df4243ae525e17157865583ae4175139c83971886c63accac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Blood-Brain Barrier</topic><topic>Brain - pathology</topic><topic>Cell Adhesion</topic><topic>Endothelium, Vascular - pathology</topic><topic>Glucose - toxicity</topic><topic>Hyperglycemia - complications</topic><topic>Hyperglycemia - pathology</topic><topic>Ischemic Attack, Transient - complications</topic><topic>Ischemic Attack, Transient - pathology</topic><topic>Male</topic><topic>myeloperoxidase</topic><topic>Neutrophils - pathology</topic><topic>Peroxidase - analysis</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - etiology</topic><topic>Reperfusion Injury - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, B</creatorcontrib><creatorcontrib>Ginsberg, M D</creatorcontrib><creatorcontrib>Busto, R</creatorcontrib><creatorcontrib>Li, L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Neurosciences Abstracts</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, B</au><au>Ginsberg, M D</au><au>Busto, R</au><au>Li, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperglycemia triggers massive neutrophil deposition in brain following transient ischemia in rats</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2000-01-07</date><risdate>2000</risdate><volume>278</volume><issue>1-2</issue><spage>1</spage><epage>4</epage><pages>1-4</pages><issn>0304-3940</issn><abstract>Myeloperoxidase (MPO) immunohistochemistry was used to ascertain the role of polymorphonuclear leukocytes in hyperglycemia-induced accentuation of brain injury after transient ischemia. Rats received 12.5 min of normothermic global cerebral ischemia by bilateral carotid occlusion plus hypotension. Hyperglycemia was induced before ischemia by intraperitoneal dextrose administration. Quantitative MPO immunohistochemistry was performed at 24 h and 3 days postischemia. Brains of normoglycemic-ischemic animals contained almost no MPO activity. By contrast, striking numbers of MPO-positive cells were present in brains studied 24 h after hyperglycemic ischemia, both within pial and parenchymal vessels and within the parenchyma. MPO deposition tended to subside at 3 days. These results indicate that hyperglycemia triggers the early, massive deposition of neutrophils in the postischemic brain--an event that may contribute to exacerbation of injury.</abstract><cop>Ireland</cop><pmid>10643786</pmid><doi>10.1016/S0304-3940(99)00889-7</doi><tpages>4</tpages></addata></record> |
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subjects | Animals Blood-Brain Barrier Brain - pathology Cell Adhesion Endothelium, Vascular - pathology Glucose - toxicity Hyperglycemia - complications Hyperglycemia - pathology Ischemic Attack, Transient - complications Ischemic Attack, Transient - pathology Male myeloperoxidase Neutrophils - pathology Peroxidase - analysis Rats Rats, Wistar Reperfusion Injury - etiology Reperfusion Injury - pathology |
title | Hyperglycemia triggers massive neutrophil deposition in brain following transient ischemia in rats |
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