{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T05:43:10Z","timestamp":1780638190220,"version":"3.54.1"},"reference-count":27,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[1983,3,1]],"date-time":"1983-03-01T00:00:00Z","timestamp":415324800000},"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":[[1983,3]]},"abstract":"<jats:p>\n                    The objective of the present study was to discover whether or not intracellular alkalosis develops in the brain in the recovery period following transient ischemia. Forebrain ischemia of 15-min duration was induced by four-vessel occlusion in rats, with recovery periods of 15, 60, and 180 min. Intracellular pH was derived both by the HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    \u2013H\n                    <jats:sub>2<\/jats:sub>\n                    CO\n                    <jats:sub>3<\/jats:sub>\n                    method and from the creatine kinase equilibrium. The ischemia was associated with energy failure and marked accumulation of lactic acid in the cerebral cortex. Recirculation brought about rapid rephosphorylation of adenine nucleotides and gradual normalization of lactic acid levels. After 15 min of recovery, the HCO\n                    <jats:sub>3<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    \u2013H\n                    <jats:sub>2<\/jats:sub>\n                    CO\n                    <jats:sub>3<\/jats:sub>\n                    method indicated persisting acidosis, but the creatine kinase reaction did not. After 60 min, a shift of pH in the alkaline direction was demonstrated in both methods. This alkalosis had disappeared after 3 h of recovery. It is concluded that resumption of ATP production after ischemia is followed by a rapid rise in intracellular pH, which transiently increases above normal.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.1983.13","type":"journal-article","created":{"date-parts":[[2011,4,8]],"date-time":"2011-04-08T13:27:23Z","timestamp":1302269243000},"page":"109-114","source":"Crossref","is-referenced-by-count":115,"title":["Intracellular pH in the Brain following Transient Ischemia"],"prefix":"10.1177","volume":"3","author":[{"given":"Hideo","family":"Mabe","sequence":"first","affiliation":[{"name":"Laboratory for Experimental Brain Research, University of Lund, Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Photjanee","family":"Blomqvist","sequence":"additional","affiliation":[{"name":"Laboratory for Experimental Brain Research, University of Lund, Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo K.","family":"Siesj\u00f6","sequence":"additional","affiliation":[{"name":"Laboratory for Experimental Brain Research, University of Lund, Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[1983,3,1]]},"reference":[{"key":"bibr1-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1097\/00000542-198003000-00002"},{"key":"bibr2-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1972.tb01309.x"},{"key":"bibr3-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.8.1.77"},{"key":"bibr4-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410080310"},{"key":"bibr5-jcbfm.1983.13","first-page":"515","volume-title":"The Enzymes","volume":"6","author":"Kuby SA","year":"1962"},{"key":"bibr6-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1977.tb07709.x"},{"key":"bibr7-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(74)91050-6"},{"key":"bibr8-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(74)90782-3"},{"key":"bibr9-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1973.tb07582.x"},{"key":"bibr10-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1973.tb00283.x"},{"key":"bibr11-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.3171\/jns.1975.43.3.0318"},{"key":"bibr12-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1970.tb04778.x"},{"key":"bibr13-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.9.4.327"},{"key":"bibr14-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1978.tb06553.x"},{"key":"bibr15-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.9.4.335"},{"key":"bibr16-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1981.9"},{"key":"bibr17-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(81)91068-4"},{"key":"bibr18-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1966.tb03294.x"},{"key":"bibr19-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1973.tb07567.x"},{"key":"bibr20-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.10.3.267"},{"key":"bibr21-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410110510"},{"key":"bibr22-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1981.34"},{"key":"bibr23-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.61.3.1079"},{"key":"bibr24-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.12.2.236"},{"key":"bibr25-jcbfm.1983.13","volume-title":"Brain Energy Metabolism","author":"Siesj\u00f6 BK","year":"1978"},{"key":"bibr26-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1981.18"},{"key":"bibr27-jcbfm.1983.13","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1972.tb01308.x"}],"container-title":["Journal of Cerebral Blood Flow &amp; 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