{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T07:21:51Z","timestamp":1777792911292,"version":"3.51.4"},"reference-count":35,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[1992,11,1]],"date-time":"1992-11-01T00:00:00Z","timestamp":720576000000},"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":[[1992,11]]},"abstract":"<jats:p>\n                    The effects of dichloroacetate (DCA) on brain lactate, intracellular pH (pH\n                    <jats:sub>i<\/jats:sub>\n                    ), phosphocreatine (PCr), and ATP during 60 min of complete cerebral ischemia and 2 h of reperfusion were investigated in rats by in vivo\n                    <jats:sup>1<\/jats:sup>\n                    H and\n                    <jats:sup>31<\/jats:sup>\n                    P magnetic resonance spectroscopy; brain lactate, water content, cations, and amino acids were measured in vitro after reperfusion. DCA, 100 mg\/kg, or saline was infused before or immediately after the ischemic period. Preischemic treatment with DCA did not affect brain lactate or pH\n                    <jats:sub>i<\/jats:sub>\n                    during ischemia, but reduced lactate and increased pH\n                    <jats:sub>i<\/jats:sub>\n                    after 30 min of reperfusion ( p &lt; 0.05 vs. controls) and facilitated the recovery of PCr and ATP during reperfusion. Postischemic DCA treatment also reduced brain lactate and increased pH\n                    <jats:sub>i<\/jats:sub>\n                    during reperfusion compared with controls ( p &lt; 0.05), but had little effect on PCr, ATP, or P\n                    <jats:sub>i<\/jats:sub>\n                    during reperfusion. After 30 min of reperfusion, serum lactate was 67% lower in the postischemic DCA group than in controls ( p &lt; 0.05). The brain lactate level in vitro was 46% lower in the postischemic DCA group than in controls ( p &lt; 0.05). DCA did not affect water content or cation concentrations in either group, but it increased brain glutamate by 40% in the preischemic treatment group ( p &lt; 0.05). The potential therapeutic effects of DCA on brain injury after complete ischemia may be mediated by reduced excitotoxin release related to decreased lactic acidosis during reperfusion.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.1992.140","type":"journal-article","created":{"date-parts":[[2011,4,8]],"date-time":"2011-04-08T13:10:21Z","timestamp":1302268221000},"page":"1030-1038","source":"Crossref","is-referenced-by-count":42,"title":["Effect of Dichloroacetate on Recovery of Brain Lactate, Phosphorus Energy Metabolites, and Glutamate during Reperfusion after Complete Cerebral Ischemia in Rats"],"prefix":"10.1177","volume":"12","author":[{"given":"Lee-Hong","family":"Chang","sequence":"first","affiliation":[{"name":"Department of Pharmaceutical Chemistry, School of Pharmacy, University of California, San Francisco, California, U.S.A."}]},{"given":"Hiroaki","family":"Shimizu","sequence":"additional","affiliation":[{"name":"Departments of Neurological Surgery, University of California, San Francisco, California, U.S.A."}]},{"given":"Hisashi","family":"Abiko","sequence":"additional","affiliation":[{"name":"Departments of Neurological Surgery, University of California, San Francisco, California, U.S.A."}]},{"given":"Raymond A.","family":"Swanson","sequence":"additional","affiliation":[{"name":"Departments of Neurology, University of California, San Francisco, California, U.S.A."}]},{"given":"Alan I.","family":"Faden","sequence":"additional","affiliation":[{"name":"Departments of Neurology, University of California, San Francisco, California, U.S.A."}]},{"given":"Thomas L.","family":"James","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Chemistry, School of Pharmacy, University of California, San Francisco, California, U.S.A."},{"name":"Departments of Radiology, School of Medicine, University of California, San Francisco, California, U.S.A."}]},{"given":"Philip 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