Acute carbon monoxide dexmedetomidine in its intoxication neuroprotective effects

Aim: It is aimed to evaluate the neuroprotective effects of Dexmedetomidine (DEX), which has antioxidant, antiapoptotic, anti-inflammatory properties, in acute carbon monoxide toxicity. Material and Method: 28 Wistar-Albino female rats were randomly divided into four groups as control, CO poisoning, CO poisoning + DEX and DEX only. The rats in the study groups were exposed to 3000 ppm CO for 30 minutes. DEX was administered half an hour after the onset of CO exposure. At the end of the experiment, blood and tissue samples were taken from the sacrificed rats. Bcl-2 Immunopositive cell values in tissue samples taken from prefrontal and hippocampal areas were scored by examining immune expressions of Bcl-2 antibodies obtained by immunohistochemical method under light microscope. MDA, NO, ADMA levels, SOD and CAT activity values were measured from blood and right hemisphere brain tissue samples by biochemical methods. Results: CAT, SOD, MDA, ADMA and NO values were statistically different between the experimental groups (p<0,001). According to the post-hoc pairwise comparison test results, there was no statistical difference in any parameter between the DEX group alone and the control group (p>0,05). CAT, SOD and NO and Bcl-2 immunosuppressive cell levels were decreased in the CO group compared to the control group (p<0,001 in all), while ADMA and MDA levels increased (p<0,001 in all). CAT, SOD and NO levels were statistically higher in the CO + DEX group compared to the CO group (p:0,007; p:0,028; p:0,017, respectively). Conclusion: DEX administered half an hour after CO poisoning increases antioxidant structures such as CAT, SOD and NO.Accordingly, DEX may have a neuroprotective effect for carbon monoxide poisoning. Keywords: Dexmedetomidine, Carbon monoxide, Neuroprotective effect