Neuroprotective effects and suppression of ischemia-induced glutamate elevation by β1-adrenoreceptor antagonists administered before transient focal ischemia in rats
β-Adrenoreceptor antagonists provide neuroprotective effects after focal cerebral ischemia in experimental settings. This study was conducted to compare the neuroprotective effects of low-dose and high-dose of selective β1-adrenoreceptor antagonists in rats after focal cerebral ischemia. We also inv...
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| Veröffentlicht in: | Journal of neurosurgical anesthesiology 2011-04, Vol.23 (2), p.131-137 |
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| creator | Goyagi, Toru Nishikawa, Toshiaki Tobe, Yoshitsugu |
| description | β-Adrenoreceptor antagonists provide neuroprotective effects after focal cerebral ischemia in experimental settings. This study was conducted to compare the neuroprotective effects of low-dose and high-dose of selective β1-adrenoreceptor antagonists in rats after focal cerebral ischemia. We also investigated whether glutamate and norepinephrine contribute to neuroprotection of the β-adrenoreceptor antagonists.
Sprague-Dawley rats were subjected to 120 minutes middle cerebral artery occlusion. The rats received intravenous infusion of saline 0.5 mL/h, esmolol 200, esmolol 2000, landiolol 50, or landiolol 500 μg/kg/min. Infusion of all the drugs were started 30 minutes before ischemia and continued for 24 hours. Neurological deficit scores were evaluated at 1, 4, and 7 days, whereas the brains were removed and stained at 7 days after ischemia. In the esmolol 200, and landiolol 50 μg/kg/min groups of additional rats, glutamate and norepinephrine concentrations in the striatum were measured separately by microdialysis during ischemia (glutamate, 120 min; norepinephrine, 110 min) and reperfusion (40 min).
Neurological deficit scores were smaller in rats treated with esmolol or landiolol than in saline-treated rats at 1, 4, and 7 days. The cortical and striatal infarct volumes were smaller in rats receiving β-adrenoreceptor antagonists than in the saline-treated rats. There were no significant differences in neurological score or infarct volume between the groups receiving the different doses of β1-adrenoreceptor antagonists. The area under the curve of glutamate in the esmolol-treated or landiolol-treated rats was significantly smaller than that in the saline-treated rats, whereas no significant differences were noted in the norepinephrine concentration among the groups.
This study indicates that the improvement in neurological and histologic outcomes by selective β1-adrenoreceptor antagonists after transient focal cerebral ischemia is partly attributed to attenuation of glutamate release. |
| doi_str_mv | 10.1097/ANA.0b013e31820369c1 |
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Sprague-Dawley rats were subjected to 120 minutes middle cerebral artery occlusion. The rats received intravenous infusion of saline 0.5 mL/h, esmolol 200, esmolol 2000, landiolol 50, or landiolol 500 μg/kg/min. Infusion of all the drugs were started 30 minutes before ischemia and continued for 24 hours. Neurological deficit scores were evaluated at 1, 4, and 7 days, whereas the brains were removed and stained at 7 days after ischemia. In the esmolol 200, and landiolol 50 μg/kg/min groups of additional rats, glutamate and norepinephrine concentrations in the striatum were measured separately by microdialysis during ischemia (glutamate, 120 min; norepinephrine, 110 min) and reperfusion (40 min).
Neurological deficit scores were smaller in rats treated with esmolol or landiolol than in saline-treated rats at 1, 4, and 7 days. The cortical and striatal infarct volumes were smaller in rats receiving β-adrenoreceptor antagonists than in the saline-treated rats. There were no significant differences in neurological score or infarct volume between the groups receiving the different doses of β1-adrenoreceptor antagonists. The area under the curve of glutamate in the esmolol-treated or landiolol-treated rats was significantly smaller than that in the saline-treated rats, whereas no significant differences were noted in the norepinephrine concentration among the groups.
This study indicates that the improvement in neurological and histologic outcomes by selective β1-adrenoreceptor antagonists after transient focal cerebral ischemia is partly attributed to attenuation of glutamate release.</description><identifier>ISSN: 0898-4921</identifier><identifier>EISSN: 1537-1921</identifier><identifier>DOI: 10.1097/ANA.0b013e31820369c1</identifier><identifier>PMID: 21150456</identifier><language>eng</language><publisher>United States</publisher><subject>Adrenergic beta-1 Receptor Antagonists - pharmacology ; Animals ; Behavior, Animal - drug effects ; Blood Gas Analysis ; Body Temperature - physiology ; Brain Chemistry - drug effects ; Consciousness Disorders - chemically induced ; Consciousness Disorders - psychology ; Extracellular Space - drug effects ; Extracellular Space - metabolism ; Gait Disorders, Neurologic - etiology ; Gait Disorders, Neurologic - psychology ; Glutamic Acid - metabolism ; Hemodynamics - physiology ; Infarction, Middle Cerebral Artery - pathology ; Ischemic Attack, Transient - drug therapy ; Ischemic Attack, Transient - metabolism ; Male ; Microdialysis ; Morpholines - pharmacology ; Neuroprotective Agents ; Norepinephrine - metabolism ; Pain Threshold - drug effects ; Propanolamines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reflex - drug effects ; Urea - analogs & derivatives ; Urea - pharmacology</subject><ispartof>Journal of neurosurgical anesthesiology, 2011-04, Vol.23 (2), p.131-137</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c221t-f25d79eba26fcecf1681ecdd4f14da33a82c69a1fd9c40e33897ac4849f3fef33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21150456$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goyagi, Toru</creatorcontrib><creatorcontrib>Nishikawa, Toshiaki</creatorcontrib><creatorcontrib>Tobe, Yoshitsugu</creatorcontrib><title>Neuroprotective effects and suppression of ischemia-induced glutamate elevation by β1-adrenoreceptor antagonists administered before transient focal ischemia in rats</title><title>Journal of neurosurgical anesthesiology</title><addtitle>J Neurosurg Anesthesiol</addtitle><description>β-Adrenoreceptor antagonists provide neuroprotective effects after focal cerebral ischemia in experimental settings. This study was conducted to compare the neuroprotective effects of low-dose and high-dose of selective β1-adrenoreceptor antagonists in rats after focal cerebral ischemia. We also investigated whether glutamate and norepinephrine contribute to neuroprotection of the β-adrenoreceptor antagonists.
Sprague-Dawley rats were subjected to 120 minutes middle cerebral artery occlusion. The rats received intravenous infusion of saline 0.5 mL/h, esmolol 200, esmolol 2000, landiolol 50, or landiolol 500 μg/kg/min. Infusion of all the drugs were started 30 minutes before ischemia and continued for 24 hours. Neurological deficit scores were evaluated at 1, 4, and 7 days, whereas the brains were removed and stained at 7 days after ischemia. In the esmolol 200, and landiolol 50 μg/kg/min groups of additional rats, glutamate and norepinephrine concentrations in the striatum were measured separately by microdialysis during ischemia (glutamate, 120 min; norepinephrine, 110 min) and reperfusion (40 min).
Neurological deficit scores were smaller in rats treated with esmolol or landiolol than in saline-treated rats at 1, 4, and 7 days. The cortical and striatal infarct volumes were smaller in rats receiving β-adrenoreceptor antagonists than in the saline-treated rats. There were no significant differences in neurological score or infarct volume between the groups receiving the different doses of β1-adrenoreceptor antagonists. The area under the curve of glutamate in the esmolol-treated or landiolol-treated rats was significantly smaller than that in the saline-treated rats, whereas no significant differences were noted in the norepinephrine concentration among the groups.
This study indicates that the improvement in neurological and histologic outcomes by selective β1-adrenoreceptor antagonists after transient focal cerebral ischemia is partly attributed to attenuation of glutamate release.</description><subject>Adrenergic beta-1 Receptor Antagonists - pharmacology</subject><subject>Animals</subject><subject>Behavior, Animal - drug effects</subject><subject>Blood Gas Analysis</subject><subject>Body Temperature - physiology</subject><subject>Brain Chemistry - drug effects</subject><subject>Consciousness Disorders - chemically induced</subject><subject>Consciousness Disorders - psychology</subject><subject>Extracellular Space - drug effects</subject><subject>Extracellular Space - metabolism</subject><subject>Gait Disorders, Neurologic - etiology</subject><subject>Gait Disorders, Neurologic - psychology</subject><subject>Glutamic Acid - metabolism</subject><subject>Hemodynamics - physiology</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Ischemic Attack, Transient - drug therapy</subject><subject>Ischemic Attack, Transient - metabolism</subject><subject>Male</subject><subject>Microdialysis</subject><subject>Morpholines - pharmacology</subject><subject>Neuroprotective Agents</subject><subject>Norepinephrine - metabolism</subject><subject>Pain Threshold - drug effects</subject><subject>Propanolamines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reflex - drug effects</subject><subject>Urea - analogs & derivatives</subject><subject>Urea - pharmacology</subject><issn>0898-4921</issn><issn>1537-1921</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1uFTEQhC0EIo_ADRDyjtUEtz1_Xj5F_ElR2MB61GO3g9GMPdieSLkQB-AgnAk_JWTBqmtRVd3qj7HXIC5A6OHd8fp4IWYBihSMUqheG3jCDtCpoQEt4Sk7iFGPTVv1GXuR8w8hhJbd8JydSYBOtF1_YL-uaU9xS7GQKf6WODlXVeYYLM_7tiXK2cfAo-M-m--0emx8sLshy2-WveCKpaYWusVy8s13_M9vaNAmCjGRoa3EVNsK3sTg86nZrv6kKNWKmVx18ZIwZE-hcBcNLo-ruA88Yckv2TOHS6ZXD_Ocffvw_uvlp-bqy8fPl8erxkgJpXGys4OmGWXvDBkH_QhkrG0dtBaVwlGaXiM4q00rSKlRD2jasdVOOXJKnbO39731Iz93ymVa6ym0LBgo7nkau34YhIC2Ott7p0kx50Ru2pJfMd1NIKYToKkCmv4HVGNvHhbs80r2MfSPiPoLAbyT0w</recordid><startdate>201104</startdate><enddate>201104</enddate><creator>Goyagi, Toru</creator><creator>Nishikawa, Toshiaki</creator><creator>Tobe, Yoshitsugu</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201104</creationdate><title>Neuroprotective effects and suppression of ischemia-induced glutamate elevation by β1-adrenoreceptor antagonists administered before transient focal ischemia in rats</title><author>Goyagi, Toru ; Nishikawa, Toshiaki ; Tobe, Yoshitsugu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c221t-f25d79eba26fcecf1681ecdd4f14da33a82c69a1fd9c40e33897ac4849f3fef33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adrenergic beta-1 Receptor Antagonists - pharmacology</topic><topic>Animals</topic><topic>Behavior, Animal - drug effects</topic><topic>Blood Gas Analysis</topic><topic>Body Temperature - physiology</topic><topic>Brain Chemistry - drug effects</topic><topic>Consciousness Disorders - chemically induced</topic><topic>Consciousness Disorders - psychology</topic><topic>Extracellular Space - drug effects</topic><topic>Extracellular Space - metabolism</topic><topic>Gait Disorders, Neurologic - etiology</topic><topic>Gait Disorders, Neurologic - psychology</topic><topic>Glutamic Acid - metabolism</topic><topic>Hemodynamics - physiology</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Ischemic Attack, Transient - drug therapy</topic><topic>Ischemic Attack, Transient - metabolism</topic><topic>Male</topic><topic>Microdialysis</topic><topic>Morpholines - pharmacology</topic><topic>Neuroprotective Agents</topic><topic>Norepinephrine - metabolism</topic><topic>Pain Threshold - drug effects</topic><topic>Propanolamines - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reflex - drug effects</topic><topic>Urea - analogs & derivatives</topic><topic>Urea - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goyagi, Toru</creatorcontrib><creatorcontrib>Nishikawa, Toshiaki</creatorcontrib><creatorcontrib>Tobe, Yoshitsugu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurosurgical anesthesiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goyagi, Toru</au><au>Nishikawa, Toshiaki</au><au>Tobe, Yoshitsugu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective effects and suppression of ischemia-induced glutamate elevation by β1-adrenoreceptor antagonists administered before transient focal ischemia in rats</atitle><jtitle>Journal of neurosurgical anesthesiology</jtitle><addtitle>J Neurosurg Anesthesiol</addtitle><date>2011-04</date><risdate>2011</risdate><volume>23</volume><issue>2</issue><spage>131</spage><epage>137</epage><pages>131-137</pages><issn>0898-4921</issn><eissn>1537-1921</eissn><abstract>β-Adrenoreceptor antagonists provide neuroprotective effects after focal cerebral ischemia in experimental settings. This study was conducted to compare the neuroprotective effects of low-dose and high-dose of selective β1-adrenoreceptor antagonists in rats after focal cerebral ischemia. We also investigated whether glutamate and norepinephrine contribute to neuroprotection of the β-adrenoreceptor antagonists.
Sprague-Dawley rats were subjected to 120 minutes middle cerebral artery occlusion. The rats received intravenous infusion of saline 0.5 mL/h, esmolol 200, esmolol 2000, landiolol 50, or landiolol 500 μg/kg/min. Infusion of all the drugs were started 30 minutes before ischemia and continued for 24 hours. Neurological deficit scores were evaluated at 1, 4, and 7 days, whereas the brains were removed and stained at 7 days after ischemia. In the esmolol 200, and landiolol 50 μg/kg/min groups of additional rats, glutamate and norepinephrine concentrations in the striatum were measured separately by microdialysis during ischemia (glutamate, 120 min; norepinephrine, 110 min) and reperfusion (40 min).
Neurological deficit scores were smaller in rats treated with esmolol or landiolol than in saline-treated rats at 1, 4, and 7 days. The cortical and striatal infarct volumes were smaller in rats receiving β-adrenoreceptor antagonists than in the saline-treated rats. There were no significant differences in neurological score or infarct volume between the groups receiving the different doses of β1-adrenoreceptor antagonists. The area under the curve of glutamate in the esmolol-treated or landiolol-treated rats was significantly smaller than that in the saline-treated rats, whereas no significant differences were noted in the norepinephrine concentration among the groups.
This study indicates that the improvement in neurological and histologic outcomes by selective β1-adrenoreceptor antagonists after transient focal cerebral ischemia is partly attributed to attenuation of glutamate release.</abstract><cop>United States</cop><pmid>21150456</pmid><doi>10.1097/ANA.0b013e31820369c1</doi><tpages>7</tpages></addata></record> |
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| subjects | Adrenergic beta-1 Receptor Antagonists - pharmacology Animals Behavior, Animal - drug effects Blood Gas Analysis Body Temperature - physiology Brain Chemistry - drug effects Consciousness Disorders - chemically induced Consciousness Disorders - psychology Extracellular Space - drug effects Extracellular Space - metabolism Gait Disorders, Neurologic - etiology Gait Disorders, Neurologic - psychology Glutamic Acid - metabolism Hemodynamics - physiology Infarction, Middle Cerebral Artery - pathology Ischemic Attack, Transient - drug therapy Ischemic Attack, Transient - metabolism Male Microdialysis Morpholines - pharmacology Neuroprotective Agents Norepinephrine - metabolism Pain Threshold - drug effects Propanolamines - pharmacology Rats Rats, Sprague-Dawley Reflex - drug effects Urea - analogs & derivatives Urea - pharmacology |
| title | Neuroprotective effects and suppression of ischemia-induced glutamate elevation by β1-adrenoreceptor antagonists administered before transient focal ischemia in rats |
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