{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T21:33:50Z","timestamp":1787002430732,"version":"build-2736575974"},"reference-count":39,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[1994,3,1]],"date-time":"1994-03-01T00:00:00Z","timestamp":762480000000},"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":[[1994,3]]},"abstract":"<jats:p>\n                    Extracellular space (ECS) volume fraction (\u03b1), ECS tortuosity (\u03bb), and nonspecific uptake ( k\u2018), three parameters affecting the diffusion of substances in nervous tissue, were studied during ischemia and anoxia in the rat spinal cord gray matter in vivo. Progressive ischemia evoked by exsanguination, as well as anoxia evoked by respiratory or cardiac arrest, produced prominent extracellular K\n                    <jats:sup>+<\/jats:sup>\n                    and pH changes closely related to a decrease in blood pressure and amplitude of field potentials. With use of ion-selective microelectrodes, the changes in the diffusion parameters were measured by quantitative analysis of concentration-time profiles of tetramethylammonium (TMA\n                    <jats:sup>+<\/jats:sup>\n                    ) applied by iontophoresis concomitantly with ionic shifts. Under normoxic conditions (in rats with blood pressure of 80\u2013110 mm Hg) diffusion parameters in the dorsal horn gray matter at depth 500\u2013900 \u03bcm were as follows: \u03b1 = 0.20 \u00b1 0.019, \u03bb = 1.62 \u00b1 0.12, k\u2019 = 4.6 \u00b1 2.5 \u00d7 10\n                    <jats:sup>\u22123<\/jats:sup>\n                    s\n                    <jats:sup>\u22121<\/jats:sup>\n                    (mean \u00b1 SD, n = 39). Extracellular K\n                    <jats:sup>+<\/jats:sup>\n                    , pH, and diffusion properties gradually changed during progressive ischemia. As the blood pressure fell to 50\u201360 mm Hg and field potential amplitude to 20\u201360%, K\n                    <jats:sup>+<\/jats:sup>\n                    rose to 6\u201312 m M, pH\n                    <jats:sub>e<\/jats:sub>\n                    fell by \u223c0.05\u20130.1 pH unit, and volume fraction of the ECS significantly decreased, to \u03b1 = 0.16 \u00b1 0.019 (n = 22). Even though the tortuosity remained virtually constant, the nonspecific uptake significantly decreased to k\u2018 = 3.4 \u00b1 1.8 \u00d7 10\n                    <jats:sup>\u22123<\/jats:sup>\n                    s\n                    <jats:sup>\u22121<\/jats:sup>\n                    . As the blood pressure fell to 20\u201330 mm Hg and field potential amplitude to 0\u20136%, K\n                    <jats:sup>+<\/jats:sup>\n                    rose to 60\u201370 m M, pH\n                    <jats:sub>e<\/jats:sub>\n                    fell by \u223c0.6\u20130.8 pH unit, and all three diffusion parameters significantly changed. The ECS volume fraction decreased to \u03b1 = 0.05 \u00b1 0.021, tortuosity increased to \u03bb = 2.00 \u00b1 0.24, and TMA\n                    <jats:sup>+<\/jats:sup>\n                    uptake decreased to k\u2019 = 1.5 \u00b1 1.6 \u00d7 10\n                    <jats:sup>\u22123<\/jats:sup>\n                    s\n                    <jats:sup>\u22121<\/jats:sup>\n                    (n = 12). No further increase in extracellular K\n                    <jats:sup>+<\/jats:sup>\n                    or changes in the \u03b1 were found during and up to 120 min after the death of the animal. However, there was a further significant increase in \u03bb = 2.20 \u00b1 0.14 and decrease in k\u2018 = 0.4 \u00b1 0.3 \u00d7 10\n                    <jats:sup>\u22123<\/jats:sup>\n                    s\n                    <jats:sup>\u22121<\/jats:sup>\n                    (n = 24). The acid shift reached its maximum level at \u223c5\u201310 min after respiratory arrest and then the pH\n                    <jats:sub>e<\/jats:sub>\n                    gradually increased by \u223c0.2 unit. Full recovery to \u201cnormoxic\u201d diffusion parameters was achieved after reinjection of the blood or after an injection of noradrenaline during severe ischemia, if this resulted in a rise in blood pressure above 80 mm Hg and a decrease in extracellular K\n                    <jats:sup>+<\/jats:sup>\n                    below 12 m M. At \u223c10 and 30 min after this recovery, the ECS volume fraction significantly increased above \u201cnormoxic\u201d values, to \u03b1 = 0.25 \u00b1 0.016 (n = 7) and \u03b1 = 0.30 \u00b1 0.021 (n = 6), respectively. The \u03bb and k\u2019 were not significantly different from the values found under normoxic conditions. Our data represent the first detailed in vivo measurements of diffusion parameters \u03b1, \u03bb, and k\u2018 during and after progressive ischemia and anoxia. The observed substantial changes in the diffusion parameters could affect the diffusion and aggravate the accumulation of ions, neurotransmitters, metabolic substances, and drugs used in therapy of nervous diseases and thus contribute to ischemic CNS damage.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.1994.37","type":"journal-article","created":{"date-parts":[[2011,4,8]],"date-time":"2011-04-08T13:17:58Z","timestamp":1302268678000},"page":"301-311","source":"Crossref","is-referenced-by-count":156,"title":["Extracellular Volume Fraction and Diffusion Characteristics during Progressive Ischemia and Terminal Anoxia in the Spinal Cord of the Rat"],"prefix":"10.1177","volume":"14","author":[{"given":"Eva","family":"Sykov\u00e1","sequence":"first","affiliation":[{"name":"Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josef","family":"Svoboda","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji\u0159\u00ed","family":"Pol\u00e1k","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandr","family":"Chv\u00e1tal","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[1994,3,1]]},"reference":[{"key":"bibr1-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1002\/glia.440030302"},{"key":"bibr2-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1989.tb07252.x"},{"key":"bibr3-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1007\/BF00364173"},{"key":"bibr4-jcbfm.1994.37","first-page":"203","volume":"37","author":"Chv\u00e1tal A","year":"1988","journal-title":"Physiol Bohemoslov"},{"key":"bibr5-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1992.112"},{"key":"bibr6-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1985.65.1.101"},{"key":"bibr7-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1980.tb06544.x"},{"key":"bibr8-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1161\/01.STR.8.4.512"},{"key":"bibr9-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1016\/S0079-6123(08)61740-9"},{"key":"bibr10-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1097\/00005072-196701000-00001"},{"key":"bibr11-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.490190415"},{"key":"bibr12-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4615-9224-2_3"},{"key":"bibr13-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1974.sp010507"},{"key":"bibr14-jcbfm.1994.37","first-page":"618","volume-title":"Rhythmogenesis in Neurons and Networks","author":"Lehmenk\u00fchler A","year":"1992"},{"key":"bibr15-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(93)90503-8"},{"key":"bibr16-jcbfm.1994.37","first-page":"115","volume":"252","author":"Lipton P","year":"1973","journal-title":"J Physiol (Lond)"},{"key":"bibr17-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1992.tb09449.x"},{"key":"bibr18-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1126\/science.2382142"},{"key":"bibr19-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1977.57.3.510"},{"key":"bibr20-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(85)90024-4"},{"key":"bibr21-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1139\/y92-278"},{"key":"bibr22-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1981.sp013981"},{"key":"bibr23-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1139\/y87-170"},{"key":"bibr24-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1385\/0-89603-115-2:247"},{"key":"bibr25-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(79)90254-3"},{"key":"bibr26-jcbfm.1994.37","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1991.65.2.264"},{"key":"bibr27-jcbfm.1994.37","doi-asserted-by":"crossref","unstructured":"Rice ME, Okada Y, Nicholson C, (1993) Anisotropic and heterogeneous diffusion in the turtle cerebellum: Implications for volume transmission. 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