Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
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Kraitsy, K; Uecal, M; Grossauer, S; Bruckmann, L; Pfleger, F; Ropele, S; Fazekas, F; Gruenbacher, G; Patz, S; Absenger, M; Porubsky, C; Smolle-Juettner, F; Tezer, I; Molcanyi, M; Fasching, U; Schaefer, U.
Repetitive long-term hyperbaric oxygen treatment (HBOT) administered after experimental traumatic brain injury in rats induces significant remyelination and a recovery of sensorimotor function.
PLoS One. 2014; 9(5): e97750-e97750.
Doi: 10.1371/journal.pone.0097750
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- Führende Autor*innen der Med Uni Graz
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Kraitsy Klaus
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Schäfer Ute
- Co-Autor*innen der Med Uni Graz
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Absenger-Novak Markus
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Bruckmann Lukas
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Fazekas Franz
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Grossauer Stefan
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Grünbacher Gerda
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Molcanyi Marek
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Patz Silke
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Porubsky Christian
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Ropele Stefan
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Smolle-Juettner Freyja-Maria
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Ücal Muammer
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Zefferer Ulrike
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- Abstract:
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Cells in the central nervous system rely almost exclusively on aerobic metabolism. Oxygen deprivation, such as injury-associated ischemia, results in detrimental apoptotic and necrotic cell loss. There is evidence that repetitive hyperbaric oxygen therapy (HBOT) improves outcomes in traumatic brain-injured patients. However, there are no experimental studies investigating the mechanism of repetitive long-term HBOT treatment-associated protective effects. We have therefore analysed the effect of long-term repetitive HBOT treatment on brain trauma-associated cerebral modulations using the lateral fluid percussion model for rats. Trauma-associated neurological impairment regressed significantly in the group of HBO-treated animals within three weeks post trauma. Evaluation of somatosensory-evoked potentials indicated a possible remyelination of neurons in the injured hemisphere following HBOT. This presumption was confirmed by a pronounced increase in myelin basic protein isoforms, PLP expression as well as an increase in myelin following three weeks of repetitive HBO treatment. Our results indicate that protective long-term HBOT effects following brain injury is mediated by a pronounced remyelination in the ipsilateral injured cortex as substantiated by the associated recovery of sensorimotor function.
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Animals -
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Brain - pathology
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Brain Injuries - pathology
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Evoked Potentials -
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Hyperbaric Oxygenation -
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Male -
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Myelin Sheath - physiology
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Psychomotor Performance -
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Rats -
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Rats, Sprague-Dawley -
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Recovery of Function -
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Time Factors -