{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T18:36:30Z","timestamp":1785868590961,"version":"3.56.0"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1995,3]]},"abstract":"<jats:p>\n            <jats:italic>Background and Purpose<\/jats:italic>\n            To facilitate reproducible and rigorous study of a tissue zone at risk of encroaching ischemic damage, we propose a new model in which the potentially compromised tissue lies within rather than perifocal to an ischemic locus. The perimeter of the \u201czone at risk\u201d is defined by a photothrombotically produced cortical lesion in the shape of a toroid (or \u201cring\u201d).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods<\/jats:italic>\n            The exposed crania of erythrosin B\u2013injected rats were irradiated with a 514.5-nm laser beam, configured as a 5-mm-diameter ring, to yield a ring-shaped lesion caused by photochemically induced platelet occlusion of cortical vasculature. Developing perfusion deficits in the interior region were revealed by carbon black infusion. Tissue damage and infarct volumes were assessed by light and electron microscopy, and blood-brain barrier integrity was assessed with Evans blue dye and horseradish peroxidase as tracers.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Results<\/jats:italic>\n            For rats injected with 17 mg\/kg erythrosin B and irradiated for 2 minutes with a ring beam intensity of 0.92 W\/cm\n            <jats:sup>2<\/jats:sup>\n            (beam power of 65 mW), carbon black infusion at times up to 4 hours demonstrated a shallow cortical ring lesion encircling a fully patent zone at risk, which by 24 hours evinced an essentially complete perfusion deficit. At times up to 24 hours, the ring lesion was penetrated at the pial surface by distal branches of the middle cerebral and anterior cerebral arteries. Stereotaxically based histopathological assessment showed that by 24 hours the lesion spanned the cortical thickness. Lesion volume increased from 14.5\u00b18.0 mm\n            <jats:sup>3<\/jats:sup>\n            (mean\u00b1SD) (n=8) to 46.2\u00b115.6 mm\n            <jats:sup>3<\/jats:sup>\n            (n=8) between 4 and 24 hours after irradiation (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01), but the anteroposterior lesion diameter did not change significantly between 4 hours (6.00\u00b11.03 mm; n=9) and 24 hours (6.75\u00b11.15 mm; n=9).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            The present model of slowly developing but inevitable cortical tissue death in a sequestered area should facilitate more precise observations of the evolution of tissue metabolic responses, from the impending onset of ischemia to the threshold of irreversible damage. This system may prove efficient for evaluating treatments intended to salvage a penumbral region.\n          <\/jats:p>","DOI":"10.1161\/01.str.26.3.444","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"444-450","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":63,"title":["A Photothrombotic \u2018Ring\u2019 Model of Rat Stroke-in-Evolution Displaying Putative Penumbral Inversion"],"prefix":"10.1161","volume":"26","author":[{"given":"Per","family":"Wester","sequence":"first","affiliation":[{"name":"From the Cerebral Vascular Disease Research Center, Department of Neurology, and the Departments of Biomedical Engineering (B.D.W.) and Anatomy and Cell Biology (W.D.D.), University of Miami (Fla)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brant D.","family":"Watson","sequence":"additional","affiliation":[{"name":"From the Cerebral Vascular Disease Research Center, Department of Neurology, and the Departments of Biomedical Engineering (B.D.W.) and Anatomy and Cell Biology (W.D.D.), University of Miami (Fla)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ricardo","family":"Prado","sequence":"additional","affiliation":[{"name":"From the Cerebral Vascular Disease Research Center, Department of Neurology, and the Departments of Biomedical Engineering (B.D.W.) and Anatomy and Cell Biology (W.D.D.), University of Miami (Fla)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. Dalton","family":"Dietrich","sequence":"additional","affiliation":[{"name":"From the Cerebral Vascular Disease Research Center, Department of Neurology, and the Departments of Biomedical Engineering (B.D.W.) and Anatomy and Cell Biology (W.D.D.), University of Miami (Fla)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410140307"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.23.11.1440719"},{"key":"e_1_3_2_3_2","first-page":"557","volume":"14","year":"1987","unstructured":"Hakim AM. The cerebral ischemic penumbra. Can J Neurol Sci. 1987;14:557-559.","journal-title":"Can J Neurol Sci"},{"key":"e_1_3_2_4_2","unstructured":"Hossmann K-A. Pathophysiology of cerebral infarction. In: Vinken PJ Bruyn GW Klawans HL eds. Handbook of Clinical Neurology. New York NY: Elsevier Science Publishing Co; 1988:107-153."},{"key":"e_1_3_2_5_2","doi-asserted-by":"crossref","unstructured":"Symon L. The relationship between CBF evoked potentials and the clinical features in cerebral ischemia. Acta Neurol Scand. 1980; 62:175-190.","DOI":"10.1111\/j.1600-0404.1980.tb05436.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00693778"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0022-510X(77)90014-4"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.12.6.6272455"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1983.12"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410150608"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00229002"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410170513"},{"key":"e_1_3_2_13_2","doi-asserted-by":"crossref","unstructured":"Dietrich WD Busto R Watson BD Scheinberg P Ginsberg MD. Photochemically induced cerebral infarction II: edema and blood-brain barrier disruption. Acta Neuropathol (Berl). 1987; 72:326-334.","DOI":"10.1007\/BF00687263"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1988.11"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1989.115"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.20.12.2688195"},{"key":"e_1_3_2_17_2","first-page":"286","volume":"24","year":"1992","unstructured":"Markgraf CG, Kraydieh S, Prado R, Watson BD, Dietrich WD, Ginsberg MD. Comparative histopathological consequences of photothrombotic occlusion of the distal middle cerebral artery in Sprague-Dawley and Wistar rats. Stroke. 1992;24:286-293.","journal-title":"Stroke"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.23.4.1561688"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1990.147"},{"key":"e_1_3_2_20_2","doi-asserted-by":"crossref","unstructured":"Cameron T Prado R Watson BD Gonzalez-Carvajal M Holets V. 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Arch Ophthalmol. 1988; 106:680-685.","DOI":"10.1001\/archopht.1988.01060130742036"},{"key":"e_1_3_2_26_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.24.10.8378958"},{"key":"e_1_3_2_27_2","doi-asserted-by":"crossref","unstructured":"Dietrich WD Prado R Halley M Watson BD. Microvascular and neuronal consequences of common carotid artery thrombosis and platelet embolization in rats. J Neuropathol Exp Neurol. 1993; 52:351-360.","DOI":"10.1097\/00005072-199307000-00002"},{"key":"e_1_3_2_28_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(08)63259-8"},{"key":"e_1_3_2_29_2","doi-asserted-by":"publisher","DOI":"10.1161\/str.23.6.1595108"},{"key":"e_1_3_2_30_2","unstructured":"Luscher TF Vanhoutte PM. The Endothelium: Modulator of Cardiovascular Function. Boca Raton Fla: CRC Press; 1990."}],"container-title":["Stroke"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/full\/10.1161\/01.STR.26.3.444","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T22:15:32Z","timestamp":1715552132000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.STR.26.3.444"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,3]]},"references-count":30,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1995,3]]}},"alternative-id":["10.1161\/01.STR.26.3.444"],"URL":"https:\/\/doi.org\/10.1161\/01.str.26.3.444","relation":{},"ISSN":["0039-2499","1524-4628"],"issn-type":[{"value":"0039-2499","type":"print"},{"value":"1524-4628","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,3]]},"assertion":[{"value":"1994-08-30","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"1994-11-03","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"1995-03-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}