{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:18:07Z","timestamp":1777792687999,"version":"3.51.4"},"reference-count":45,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[1991,9,1]],"date-time":"1991-09-01T00:00:00Z","timestamp":683683200000},"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":[[1991,9]]},"abstract":"<jats:p>\n                    Barbiturates and the volatile anesthetic isoflurane reduce CMR to similar values. If the mechanism of barbiturate protection against focal ischemic injury is due to a reduction in cellular energy requirements, then isoflurane should similarly reduce ischemic injury. To evaluate this, spontaneously hypertensive rats underwent 2 h of reversible middle cerebral artery occlusion (MCAO) while receiving deep methohexital, isoflurane, or halothane anesthesia. Ninety-six hours postischemia, neurologic deficits were present but without a difference between groups. Mean \u00b1 SD infarct volume, as assessed by triphenyl tetrazolium chloride staining and computerized planimetry, was significantly less in the methohexital group (n = 8; 166 \u00b1 74 mm\n                    <jats:sup>3<\/jats:sup>\n                    ) than in either the halothane (n = 9; 249 \u00b1 71 mm\n                    <jats:sup>3<\/jats:sup>\n                    ; p &lt; 0.04) or the isoflurane (n = 9; 243 \u00b1 62 mm\n                    <jats:sup>3<\/jats:sup>\n                    ; p &lt; 0.03) groups. One possible explanation for the lack of protective effect for isoflurane might be related to its vasodilative properties, which could result in a cerebral vascular steal. To examine this possibility, rats anesthetized with methohexital or isoflurane underwent autoradiographic determination of CBF with or without MCAO. In isoflurane-anesthetized sham rats (n = 5; no ischemia), CBF was approximately three times greater than in methohexital-treated (n = 5) sham rats. During ischemia, although a regional reduction in flow was noted in both anesthetic groups, mean flow remained greater in the isoflurane group. When the ischemic hemisphere was analyzed for percentage of cross-sectional area where flow was &lt;25 ml\/100 g\/min, significantly less tissue appeared to be at risk for infarction in the isoflurane group (n = 7; 32.9 \u00b1 19.4%) versus the methohexital group (n = 8; 49.1 \u00b1 12.6%; p &lt; 0.05). These results are consistent with the following conclusions: (a) CMR reduction is not a sufficient criterion for anesthetic-mediated brain protection; (b) isoflurane does not cause cerebrovascular steal; and (c) ischemic flow thresholds for infarction are different for methohexital and isoflurane.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.1991.137","type":"journal-article","created":{"date-parts":[[2011,4,8]],"date-time":"2011-04-08T13:05:44Z","timestamp":1302267944000},"page":"794-802","source":"Crossref","is-referenced-by-count":83,"title":["Reversible Focal Ischemia in the Rat: Effects of Halothane, Isoflurane, and Methohexital Anesthesia"],"prefix":"10.1177","volume":"11","author":[{"given":"David S.","family":"Warner","sequence":"first","affiliation":[{"name":"Department of Anesthesia, University of Iowa, Iowa City, Iowa, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiegang","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, University of Iowa, Iowa City, Iowa, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ramachandran","family":"Ramani","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, University of Iowa, Iowa City, Iowa, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael M.","family":"Todd","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, University of Iowa, Iowa City, Iowa, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[1991,9,1]]},"reference":[{"key":"bibr1-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1990.114"},{"key":"bibr2-jcbfm.1991.137","first-page":"412","volume":"11","author":"Bederson J","year":"1986","journal-title":"Stroke"},{"key":"bibr3-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.10.6.647"},{"key":"bibr4-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1988.88"},{"key":"bibr5-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1987.127"},{"key":"bibr6-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.20.7.904"},{"key":"bibr7-jcbfm.1991.137","first-page":"H211","volume":"259","author":"Cole D","year":"1990","journal-title":"Am J Physiol"},{"key":"bibr8-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1093\/bja\/64.4.498"},{"key":"bibr9-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1097\/00000542-197406000-00011"},{"key":"bibr10-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(90)91060-T"},{"key":"bibr11-jcbfm.1991.137","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.20.11.1538"},{"key":"bibr12-jcbfm.1991.137","unstructured":"Eger E, (1974) Anesthetic Uptake and Action. 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