Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity

The goal of this investigation was to determine whether exposure to hyperbaric oxygen (HBO2) would ameliorate biochemical and functionalbrain abnormalities in an animal model of carbon monoxide (CO) poisoning. In this model, CO-mediated oxidative stress causes chemicalalterations in myelin basic protein (MBP), which initiates an adaptive immunological response that leads to a functional deficit. CO-exposed ratsdo not show improvements in task performance in a radial maze. We found that HBO2 given after CO poisoning will prevent this deficit, but noteliminate all of the CO-mediated biochemical alterations in MBP. MBP from HBO2 treated CO-exposed rats is recognized normally by a battery ofantibodies, but exhibits an abnormal charge pattern. Lymphocytes from HBO2-treated and control rats do not become activated when incubatedwith MBP, immunohistological evidence of microglial activation is not apparent, and functional deficits did not occur, unlike untreated CO exposed rats. The results indicate that HBO2 prevents immune-mediated delayed neurological dysfunction following