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The Time Dependant Protective Effect of Hyperbaric Oxygen on Neuronal Cell Apoptosis in Carbon Monoxide Poisoning

Objective: The progressive clinical course with delayed encephalopathy in carbon monoxide (CO) poisoning may be due to neuronal apoptosis. One of the key events in the process of apoptosis is the activation of caspase-3. The time dependant hyperbaric 100% oxygen (HBO) efficiency in preventing neuron...

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Published in:Clinical toxicology (Philadelphia, Pa.) Pa.), 2008-06, Vol.46 (5), p.406-406
Main Authors: Brvar, M, Luzar, B, Cor, A, Finderle, Z, Suput, D, Bunc, M
Format: Article
Language:English
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Summary:Objective: The progressive clinical course with delayed encephalopathy in carbon monoxide (CO) poisoning may be due to neuronal apoptosis. One of the key events in the process of apoptosis is the activation of caspase-3. The time dependant hyperbaric 100% oxygen (HBO) efficiency in preventing neuronal cell apoptosis after CO-poisoning is not known. The aim of our study was to evaluate HBO efficacy in preventing neuronal cell apoptosis in different time periods after CO exposure in an animal model. Methods: Wistar rats were exposed to 3,000 ppm of CO for 60 minutes. The control group was left afterwards on ambient air. The rest of the rats were grouped and exposed to HBO immediately (Group 1), 1 hour (Group 2) and 3 hours (Group 3) after CO exposure. 24 hours after CO exposure the rats were sacrificed and immunohystological analysis with antibodies against activated caspase-3 was performed to evaluate apoptosis of hip-pocampal ganglionic cells. A percentage of apoptotic ganglionic cells in the hippocampus was reported. Results: Analyses of differences in percentage of apoptotic cells between different kinds of therapy showed that the percentage of apoptotic cells of the first group (20.6 plus or minus 2.1%,) immediately treated with HBO and the second group (21.9 plus or minus 5.1%) treated with HBO 1 hour after CO exposure were similar, and both of them were significantly different, with a much lower percentage of apoptotic cells, from the control group left on ambient air (31 plus or minus 3.0%) and with a much higher percentage of apoptotic cells than the third group treated with HBO 3 hours after CO exposure (8.6 plus or minus 1.7%). Conclusions: CO-poisoning results in brain ganglionic cell apoptosis. HBO has a protective effect on CO-induced ganglionic cell apoptosis, but it seems that HBO 3 hours after CO exposure is more effective in preventing apoptosis than HBO within 1 hour after CO exposure. These results suggest the modification of currently used indications for HBO according to the time elapsed after CO exposure since immediate or premature HBO might not be so effective in preventing apoptosis. The evaluation of HBO in preventing neuronal cell apoptosis and necrosis more than 3 hours after CO poisoning is in progress.
ISSN:1556-3650