| Abstract | | Cerebral hypoxia is a major cause of morbidity and mortality afrer carbon monoxide (CO) poisoning. The criteria to use hyperbaric oxygenation therapy (hBOT) are not equivocal. Recently, many neurobiochemical markers of brain damage gained increasing interest. One of these is the protein S-100B. It was found to be elevated in unconsciousness CO-poisoned patients and was shown as a good prognostic parameter in CO-poisoned rats. The aim of this study was to evaluate S-100B protein during normobaric and hyperbaric oxygen therapy of conscious CO-poisoned rats.The rats were exposed to a mixture of 3,000 ppm CO in air for GO minutes. After CO exposure, eight rats were exposed to ambient air, six to 100% normobaric oxygen, and six to 100 % hyperbaric oxygen <3 Bar for 30 minutes. Blood samples were taken from the jugular vein just before CO exposure and immediately after therapy. The S-100B concentrations were measured with a commercial immunoluminometric assay (Liaison Sangtec 100). S-100B levels afrer therapy of the first group of rats treated with ambient air and the second group treated with normobaric oxygen were similar (0.16±0.07 wg/L vs. 0.19±0.05 pg/L, p = 0,741). Both of them were significantly different from the third group of rats treated with hyperbaric oxygen (0.06±0.03 Ng/L; p = 0,018 and p = 0,.002, respectively). S-100B is elevated in conscious CO-poisoned rats treated with ambient air or normobaric oxygen, but not in conscious CO-poisoned rats treated with hyperbaric oxygen. Key words: hyperbaric oxygen, toxicology, carbon monoxide.
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