{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,13]],"date-time":"2026-09-13T01:32:35Z","timestamp":1789263155724,"version":"build-2803163510"},"reference-count":8,"publisher":"S. Karger AG","issue":"5","license":[{"start":{"date-parts":[[2002,1,1]],"date-time":"2002-01-01T00:00:00Z","timestamp":1009843200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2002,1,1]],"date-time":"2002-01-01T00:00:00Z","timestamp":1009843200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Dev Neurosci"],"published-print":{"date-parts":[[2002]]},"abstract":"<jats:p>We hypothesized that creatine (Cr) supplementation would preserve energy metabolism and thus ameliorate the energy failure and the extent of brain edema seen after severe but transient cerebral hypoxia-ischemia (HI) in the neonatal rat model. Six-day-old (P6) rats received subcutaneous Cr monohydrate injections for 3 consecutive days (3 g\/kg body weight\/day), followed by &lt;sup&gt;31&lt;\/sup&gt;P-magnetic resonance spectroscopy (MRS) at P9. In a second group, P4 rats received the same Cr dose as above for 3 days prior to unilateral common carotid artery ligation followed 1 h later by 100 min of hypoxia (8% O&lt;sub&gt;2&lt;\/sub&gt;) at P7. Rats were maintained at 37\u00b0C rectal temperature until magnetic resonance imaging was performed 24 h after HI. Cr supplementation for 3 days significantly increased the energy potential, i.e. the ratio of phosphocreatine to \u03b2-nucleotide triphosphate (PCr\/\u03b2NTP) and PCr\/inorganic phosphate (PCr\/Pi) as measured by &lt;sup&gt;31&lt;\/sup&gt;P-MRS. Rats with hemispheric cerebral hypoxic-ischemic insult that had received Cr showed a significant reduction (25%) of the volume of edemic brain tissue compared with controls as calculated from diffusion-weighted images (DWI). Thus, prophylactic Cr supplementation demonstrated a significant neuroprotective effect 24 h after transient cerebral HI. We hypothesize that neuroprotection is probably due to the availability of a larger metabolic substrate pool leading to a reduction of the secondary energy failure because DWI has been reported to correlate with the PCr\/Pi ratio in the acute phase of injury. Additional protection by Cr may be related to prevention of calcium overload, prevention of mitochondrial permeability transition pore opening and direct antioxidant effects.<\/jats:p>","DOI":"10.1159\/000069043","type":"journal-article","created":{"date-parts":[[2003,4,15]],"date-time":"2003-04-15T12:11:24Z","timestamp":1050408684000},"page":"382-388","source":"Crossref","is-referenced-by-count":76,"title":["Neuroprotection of Creatine Supplementation in Neonatal Rats with Transient Cerebral Hypoxia-Ischemia"],"prefix":"10.1159","volume":"24","author":[{"given":"Kathryn H.","family":"Adcock","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johann","family":"Nedelcu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Loenneker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ernst","family":"Martin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theo","family":"Wallimann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bendicht P.","family":"Wagner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2003,3,21]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1542\/peds.100.6.1004"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1999.0732477.x"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2000.0741968.x"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1038\/6568"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1159\/000017473"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.275.10.6937"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1999.0720529.x"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1017\/S0012162299000171"}],"container-title":["Developmental Neuroscience"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/69043","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/69043","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T03:41:22Z","timestamp":1745466082000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000069043"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2002]]},"references-count":8,"journal-issue":{"issue":"5","published-online":{"date-parts":[[2003,3,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000069043","archive":["Portico"],"relation":{},"ISSN":["0378-5866","1421-9859"],"issn-type":[{"value":"0378-5866","type":"print"},{"value":"1421-9859","type":"electronic"}],"subject":[],"published":{"date-parts":[[2002]]}}}