{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T07:03:38Z","timestamp":1765609418294},"reference-count":51,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,8]]},"abstract":"<jats:p content-type=\"fine-print\"><jats:italic>Object.<\/jats:italic> Severe traumatic brain injury (TBI) imposes a huge metabolic load on brain tissue, which can be summarized initially as a state of hypermetabolism and hyperglycolysis. In experiments O<jats:sub>2<\/jats:sub> consumption has been shown to increase early after trauma, especially in the presence of high lactate levels and forced O<jats:sub>2<\/jats:sub> availability. In recent clinical studies the effect of increasing O<jats:sub>2<\/jats:sub> availability on brain metabolism has been analyzed. By their nature, however, clinical trauma models suffer from a heterogeneous injury distribution. The aim of this study was to analyze, in a standardized diffuse brain injury model, the effect of increasing the fraction of inspired O<jats:sub>2<\/jats:sub> on brain glucose and lactate levels, and to compare this effect with the metabolism of the noninjured sham-operated brain.<\/jats:p>\n<jats:p content-type=\"fine-print\"><jats:italic>Methods.<\/jats:italic> A diffuse severe TBI model developed by Foda and Maramarou, et al., in which a 420-g weight is dropped from a height of 2 m was used in this study. Forty-one male Wistar rats each weighing approximately 300 g were included. Anesthesized rats were monitored by placing a femoral arterial line for blood pressure and blood was drawn for a blood gas analysis. Two time periods were defined: Period A was defined as preinjury and Period B as postinjury. During Period B two levels of fraction of inspired oxygen (FiO<jats:sub>2<\/jats:sub>) were studied: air (FiO<jats:sub>2<\/jats:sub> 0.21) and oxygen (FiO<jats:sub>2<\/jats:sub> 1). Four groups were studied including sham-operated animals: air-air-sham (AAS); air-O<jats:sub>2<\/jats:sub>-sham (AOS); air-air-trauma (AAT); and air-O<jats:sub>2<\/jats:sub>-trauma (AOT). In six rats the effect of increasing the FiO<jats:sub>2<\/jats:sub> on serum glucose and lactate was analyzed.<\/jats:p>\n<jats:p content-type=\"fine-print\">During Period B lactate values in the brain determined using microdialysis were significantly lower (p &lt; 0.05) in the AOT group than in the AAT group and glucose values in the brain determined using microdialysis were significantly higher (p &lt; 0.04). No differences were demonstrated in the other groups. Increasing the FiO<jats:sub>2<\/jats:sub> had no significant effect on the serum levels of glucose and lactate.<\/jats:p>\n<jats:p content-type=\"fine-print\"><jats:italic>Conclusions.<\/jats:italic> Increasing the FiO<jats:sub>2<\/jats:sub> influences dialysate glucose and lactate levels in injured brain tissue. Using an FiO<jats:sub>2<\/jats:sub> of 1 influences brain metabolism in such a way that lactate is significantly reduced and glucose significantly increased. No changes in dialysate glucose and lactate values were found in the noninjured brain.<\/jats:p>","DOI":"10.3171\/jns.2004.101.2.0323","type":"journal-article","created":{"date-parts":[[2009,5,13]],"date-time":"2009-05-13T18:00:51Z","timestamp":1242237651000},"page":"323-329","source":"Crossref","is-referenced-by-count":25,"title":["Influence of oxygen therapy on glucose\u2014lactate metabolism after diffuse brain injury"],"prefix":"10.3171","volume":"101","author":[{"given":"Michael","family":"Reinert","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Benoit","family":"Schaller","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans 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