{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T10:50:47Z","timestamp":1785149447481,"version":"3.55.0"},"reference-count":37,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[1985,3,1]],"date-time":"1985-03-01T00:00:00Z","timestamp":478483200000},"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":[[1985,3]]},"abstract":"\n The objective of the study was to estimate changes in extracellular pH (pH\n e<\/jats:sub>\n ) and intracellular pH (pH\n i<\/jats:sub>\n ) during seizures and in the recovery period following the arrest of seizure activity. Seizures of 5- and 20-min duration were induced in rats by fluorothyl added to the insufflated gas mixture, and recovery for 5, 15, and 45 min was instituted by withdrawal of the fluorothyl supply following 20 min of continuous seizures. Changes in pH\n e<\/jats:sub>\n were measured by double-barreled, liquid ion-exchange pH microelectrodes, and in pH\n i<\/jats:sub>\n by the CO\n 2<\/jats:sub>\n method, following estimation of tissue P\n CO2<\/jats:sub>\n and extracellular fluid (ECF) volume. The animals were either normoxic or rendered moderately hypoxic (arterial Po\n 2<\/jats:sub>\n 40\u201350 mm Hg). Upon induction of seizures in normoxic animals, pH\n e<\/jats:sub>\n decreased by a mean of 0.36 unit, the values being identical at 5 and 20 min. In moderate hypoxia, seizures sustained for 20 min were accompanied by a further fall in pH\n e<\/jats:sub>\n (mean decrease 0.51 unit). The changes in pH\n e<\/jats:sub>\n seemed mainly to reflect the nonionic diffusion of lactic acid from cells to the ECF (tissue lactate levels \u223c 10 and 15 \u03bcmol g\n \u22121<\/jats:sup>\n during seizures in normoxic and hypoxic animals, respectively). However, the gradual fall in pH\n e<\/jats:sub>\n attributable to lactic acid production was preceded by rapid acidification, sometimes exceeding the steady-state values subsequently attained. This acidification was interpreted to reflect spreading depression and fast transcellular Na\n +<\/jats:sup>\n \/H\n +<\/jats:sup>\n exchange. Following cessation of seizure discharge, pH\n e<\/jats:sub>\n normalized at a surprisingly slow rate, with some acidosis persisting even after 45 min. The difference between cerebrovenous and arterial Pco\n 2<\/jats:sub>\n was reduced during seizures and increased in the recovery period, probably reflecting alterations in the blood flow\/metabolic rate coupling. Impedance changes were slight, indicating only minor changes in ECF volume. Changes in pH\n i<\/jats:sub>\n after 5 min of seizures ranged from 0.20 (normoxic animals) to 0.32 (hypoxic animals) unit, the pH\n i<\/jats:sub>\n values after 20 min being 0.07\u20130.08 unit higher. The results suggest the regulation of pH\n i<\/jats:sub>\n during ongoing seizures. Upon arrest of seizure activity, pH\n i<\/jats:sub>\n rapidly increased to normal and subsequently to supranormal values. Postepileptic intracellular alkalosis occurred at a time when pH\n e<\/jats:sub>\n was still reduced and in spite of the fact that tissue lactate values had not normalized. It is concluded that the rapid normalization of pH\n i<\/jats:sub>\n and overt alkalosis were caused by the simultaneously occurring oxidation of lactate, with the removal of a stoichiometrical amount of H\n +<\/jats:sup>\n , and the extrusion of H\n +<\/jats:sup>\n from cells, possibly via a Na\n +<\/jats:sup>\n \/H\n +<\/jats:sup>\n exchanger, the latter probably delaying normalization of pH\n e<\/jats:sub>\n .\n <\/jats:p>","DOI":"10.1038\/jcbfm.1985.7","type":"journal-article","created":{"date-parts":[[2011,4,8]],"date-time":"2011-04-08T13:29:12Z","timestamp":1302269352000},"page":"47-57","source":"Crossref","is-referenced-by-count":143,"title":["Extra- and Intracellular pH in the Brain during Seizures and in the Recovery Period following the Arrest of Seizure Activity"],"prefix":"10.1177","volume":"5","author":[{"given":"Bo K.","family":"Siesj\u00f6","sequence":"first","affiliation":[{"name":"Laboratory for Experimental Brain Research and Departments of Pediatrics and Anaesthesiology, University of Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roger","family":"von Hanwehr","sequence":"additional","affiliation":[{"name":"Laboratory for Experimental Brain Research and Departments of Pediatrics and Anaesthesiology, University of Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00f6rel","family":"Nergelius","sequence":"additional","affiliation":[{"name":"Laboratory for Experimental Brain Research and Departments of Pediatrics and Anaesthesiology, University of Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gunilla","family":"Nevander","sequence":"additional","affiliation":[{"name":"Laboratory for Experimental Brain Research and Departments of Pediatrics and Anaesthesiology, University of Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Ingvar","sequence":"additional","affiliation":[{"name":"Laboratory for Experimental Brain Research and Departments of Pediatrics and Anaesthesiology, University of Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[1985,3,1]]},"reference":[{"key":"bibr1-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1021\/ac00237a031"},{"key":"bibr2-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1002\/9780470720370.ch16"},{"key":"bibr3-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1977.tb05929.x"},{"key":"bibr4-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410050207"},{"key":"bibr5-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1967.sp008120"},{"key":"bibr6-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1974.227.5.1173"},{"key":"bibr7-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1157.1972.tb04403.x"},{"key":"bibr8-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1977.tb10665.x"},{"key":"bibr9-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1975.tb03657.x"},{"key":"bibr10-jcbfm.1985.7","volume-title":"Handbook of Physiology, Vol 2: The Respiratory System","author":"Fencl V","year":"1984"},{"key":"bibr11-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1966.210.3.459"},{"key":"bibr12-jcbfm.1985.7","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1981.tb04673.x"},{"key":"bibr13-jcbfm.1985.7","doi-asserted-by":"crossref","unstructured":"Folbergrov\u00e1 J, Ingvar M, Nevander G, Siesj\u00f6 BK, (1985) Cerebral metabolic changes during and following fluorothyl-in-duced seizures in ventilated rats. 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