{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T17:11:26Z","timestamp":1790356286268,"version":"4.1.0"},"reference-count":56,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[1994,3,1]],"date-time":"1994-03-01T00:00:00Z","timestamp":762480000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[1994,3]]},"abstract":"<jats:p>\n                    We tested the abilities of two potent non- N-methyl-d-aspartate (non-NMDA) glutamate antagonists [2,3-dihydroxy-6-nitro-7-sulfamoylbenzo( F)quinoxaline (NBQX)] and [1-(4-aminophenyl)-4-methyl-7,8-methylene-dioxy-5 H-2,3-benzodiazepine hydrochloride (GYKI 52466)] to reduce neocortical infarction following 2 h of transient middle cerebral artery occlusion in a hypertensive stroke model in the rat and compared these effects against, and in combination with, a potent NMDA antagonist [(+)-5-methyl-10,11-dihydro-5 H-dibenzo-[ a,d]cyclohepten-5,10-amine maleate (MK-801)]. In Expt. 1, an already established cytoprotective dose of Na\n                    <jats:sup>+<\/jats:sup>\n                    -NBQX (30 mg\/kg i.p. \u00d7 3) was compared with saline (1 ml), the NMDA antagonist MK-801 (1 mg\/kg i.p. \u00d7 3), and a combination of the same doses of both NBQX and MK-801. Initial doses were delayed to 90 min following occlusion with subsequent injections at the time of reperfusion and 30 min following reperfusion. Saline-treated rats sustained 181 \u00b1 32 mm\n                    <jats:sup>3<\/jats:sup>\n                    (n = 15) of neocortical infarction (mean \u00b1 SD). This was significantly reduced by NBQX to 137 \u00b1 25 mm\n                    <jats:sup>3<\/jats:sup>\n                    (n = 15, p &lt; 0.05) of damage. Neither MK-801 (170 \u00b1 33 mm\n                    <jats:sup>3<\/jats:sup>\n                    ; n = 11) nor the combination of MK-801 and NBQX (169 \u00b1 20 mm\n                    <jats:sup>3<\/jats:sup>\n                    ; n = 6) proved to be cytoprotective when given with a 90-min delay. In Expt. 2, NBQX (30 mg\/kg) was dissolved (6 mg\/ml) in 5% dextrose and compared with both saline and dextrose (1.2 ml) i.v. infusions given over a 4-h period starting 1 h after occlusion. Saline-treated rats had a mean infarct of 183 \u00b1 27 mm\n                    <jats:sup>3<\/jats:sup>\n                    (n = 6), dextrose-treated had 200 \u00b1 30 mm\n                    <jats:sup>3<\/jats:sup>\n                    (n = 9), while for NBQX-treated rats it was reduced to 129 \u00b1 60 mm\n                    <jats:sup>3<\/jats:sup>\n                    (n = 10, p &lt; 0.05). Intravenous NBQX precipitated into the renal tubules, causing nephrotoxicity. In Expt. 3, rats were given either saline (1 ml i.p.) or GYKI 52466 (10 mg\/kg i.p.) at 30 and 90 min following occlusion and at 30, 90, and 150 min following reperfusion. Saline-treated rats sustained 187 \u00b1 27 mm\n                    <jats:sup>3<\/jats:sup>\n                    of neocortical infarction (n = 7), while those treated with GYKI 52466 were protected, with 139 \u00b1 38 mm\n                    <jats:sup>3<\/jats:sup>\n                    of infarction (n = 7, p &lt; 0.05). A clinically useful role for \u03b1-amino-3-hydroxy-5-methyl-4-isoxazole propionate antagonists in embolic stroke is envisaged if nontoxic drugs can be developed, since cerebroprotection was achieved with delayed treatment with both of these lead compounds.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.1994.32","type":"journal-article","created":{"date-parts":[[2011,4,8]],"date-time":"2011-04-08T13:17:58Z","timestamp":1302268678000},"page":"251-261","source":"Crossref","is-referenced-by-count":157,"title":["Delayed Treatment with AMPA, but Not NMDA, Antagonists Reduces Neocortical Infarction"],"prefix":"10.1177","volume":"14","author":[{"given":"Dong","family":"Xue","sequence":"first","affiliation":[{"name":"Neurology-Neuroscience, Ottawa Civic Hospital, University of Ottawa, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi-Gao","family":"Huang","sequence":"additional","affiliation":[{"name":"Neurology-Neuroscience, Ottawa Civic Hospital, University of Ottawa, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kimberley","family":"Barnes","sequence":"additional","affiliation":[{"name":"Neurology-Neuroscience, Ottawa Civic Hospital, University of Ottawa, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard J.","family":"Lesiuk","sequence":"additional","affiliation":[{"name":"Neurology-Neuroscience, Ottawa Civic Hospital, University of Ottawa, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen E.","family":"Smith","sequence":"additional","affiliation":[{"name":"Neurology-Neuroscience, Ottawa Civic Hospital, University of Ottawa, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alastair M.","family":"Buchan","sequence":"additional","affiliation":[{"name":"Neurology-Neuroscience, Ottawa Civic Hospital, University of Ottawa, Ottawa, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[1994,3,1]]},"reference":[{"key":"bibr1-jcbfm.1994.32","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199203000-00004"},{"key":"bibr2-jcbfm.1994.32","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1984.tb05396.x"},{"key":"bibr3-jcbfm.1994.32","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1988.88"},{"key":"bibr4-jcbfm.1994.32","first-page":"1","volume":"2","author":"Buchan AM","year":"1990","journal-title":"Cerebrovasc Brain Metab 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