{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:39:05Z","timestamp":1761154745977},"reference-count":49,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,2,5]],"date-time":"2009-02-05T00:00:00Z","timestamp":1233792000000},"content-version":"vor","delay-in-days":3902,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[1998,6]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>We describe the effects of barbiturates on the neurotoxicity induced by nitric oxide (NO) on foetal rat cultured cortical and hippocampal neurones. Cessation of cerebral blood flow leads to an initiation of a neurotoxic cascade including NO and peroxynitrite. Barbiturates are often used to protect neurones against cerebrovascular disorders clinically. However, its neuroprotective mechanism remains unclear.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In the present experiment, we established a new <jats:italic>in vitro<\/jats:italic> model of brain injury mediated by NO with an NO\u2010donor, 1\u2010hydroxy\u20102\u2010oxo\u20103\u2010(3\u2010aminopropyl)\u20103\u2010isopropyl\u20101\u2010triazene (NOC\u20105) on grid tissue culture wells. We also investigated the mechanisms of protection of CNS neurones from NO\u2010induced neurotoxicity by thiopentone sodium, which contains a sulphhydryl group (SH\u2010) in the medium, and pentobarbitone sodium, which does not contain SH\u2010.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Primary cultures of cortical and hippocampal neurones (prepared from 16\u2010day gestational rat foetuses) were used after 13\u201314 days in culture. The cells were exposed to NOC\u20105 at the various concentrations for 24 h in the culture to evaluate a dose\u2010dependent effect of NOC\u20105.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>To evaluate the role of the barbiturates, neurones were exposed to 4, 40 and 400 \u03bc<jats:sc>M<\/jats:sc> of thiopentone sodium or pentobarbitone sodium with or without 30 \u03bc<jats:sc>M<\/jats:sc> NOC\u20105. In addition, superoxide dismutase (SOD) at 1000 u ml<jats:sup>\u22121<\/jats:sup> and 30 \u03bc<jats:sc>M<\/jats:sc> NOC\u20105 were co\u2010administered for 24 h to evaluate the role of SOD.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Exposure to NOC\u20105 induced neural cell death in a dose\u2010dependent manner in both cortical and hippocampal cultured neurones. Approximately 90% of the cultured neurones were killed by 100 \u03bc<jats:sc>M<\/jats:sc> NOC\u20105.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>This NOC\u20105\u2010induced neurotoxicity was significantly attenuated by high concentrations of thiopentone sodium (40 and 400 \u03bc<jats:sc>M<\/jats:sc>) as well as SOD, but not by pentobarbitone sodium. The survival rates of the cortical neurones and hippocampal neurones that were exposed to 30 \u03bc<jats:sc>M<\/jats:sc> NOC\u20105 were 11.2\u00b14.2% and 37.2\u00b13.0%, respectively, and in the presence of 400 \u03bc<jats:sc>M<\/jats:sc> thiopentone sodium, the survival rate increased to 65.3\u00b13.5% in the cortical neurones and 74.6\u00b12.2% in the hippocampal neurones.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>These findings demonstrate that thiopentone sodium, which acts as a free radical scavenger, protects the CNS neurones against NO\u2010mediated cytotoxicity <jats:italic>in vitro<\/jats:italic>. In conclusion, thiopentone sodium is one of the best of the currently available pharmacological agents for protection of neurones against intraoperative cerebral ischaemia.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p>","DOI":"10.1038\/sj.bjp.0701884","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T19:30:35Z","timestamp":1106940635000},"page":"804-810","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Nitric oxide\u2010induced cytotoxicity attenuation by thiopentone sodium but not pentobarbitone sodium in primary brain cultures"],"prefix":"10.1111","volume":"124","author":[{"given":"Satoshi","family":"Shibuta","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jun","family":"Kosaka","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takashi","family":"Mashimo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yutaka","family":"Fukuda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ikuto","family":"Yoshiya","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2009,2,5]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(91)90406-U"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/345027b0"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1042\/bst0210330"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1021\/ic00216a003"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.22.9030"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(95)00401-T"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.3181\/00379727-211-43950E"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.13-06-02651.1993"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.14-09-05147.1994"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199117003-00006"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(87)90493-6"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/0891-5849(88)90115-3"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(91)90022-M"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1038\/369061a0"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1995.115"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1227\/00006123-199509000-00018"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF03006535"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/0076-6879(90)86093-B"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(94)90530-4"},{"key":"e_1_2_7_21_1","doi-asserted-by":"publisher","DOI":"10.1021\/jo00058a030"},{"key":"e_1_2_7_22_1","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.1993.1067"},{"key":"e_1_2_7_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(92)90224-P"},{"key":"e_1_2_7_24_1","first-page":"260","article-title":"Glutamate receptors agonists stimulate nitric oxide synthase in primary cultures of cerebellar granule cells","volume":"45","author":"Kiedrowski L.","year":"1992","journal-title":"J. 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