Neuroprotective Effects of Dexmedetomidine in Acute Carbon Monoxide Intoxication: An Experimental Study

Abstract

Objective: 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, Carbon monoxide (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 Immunopositively 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. Malondialdehyde (MDA), nitric oxide (NO), asymmetric dimethylarginine ADMA levels, superoxide dismutase (SOD), and catalase (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

• Carbon monoxide
• Dexmedetomidine
• Neuroprotective effect

Akut Karbonmonoksit İntoksikasyonunda Deksmedetomidin’in Nöroprotektif Etkileri: Deneysel Bir Çalışma

Abstract

Amaç: Antioksidan, antiapopitotik, antiinflamatuar özellikleri olan Deksmedetomidin’in (DEX) akut karbonmonoksit (CO) toksikasyonunda nöroprotektif etkilerinin değerlendirmesi amaçlanmıştır. Gereç ve Yöntem: 28 adet Wistar-Albino dişi sıçan kontrol, CO zehirlenme, CO zehirlenme + DEX ve sadece DEX olmak üzere rastgele dört gruba ayrıldı. Çalışma gruplarındaki sıçanlar 3000 ppm konsantrasyonda CO’e 30 dakika boyunca maruz bırakıldı. DEX CO maruziyetinden yarım saat sonra uygulandı. Deney bitiminde sakrifiye edilen sıçanlardan kan ve doku örnekleri alındı. Prefrontal ve hipokampal alanlardan alınan doku örneklerinde Bcl-2 İmmunopositif hücre değerleri immunohistokimyasal yöntem ile elde edilen Bcl-2 antikorların immune ekspresyonlarının ışık mikroskobu altında incelenmesi ile skorlandı. Alınan kan ve sağ hemisfer beyin doku örneklerinden biyokimyasal yöntemlerle malondialdehit (MDA), nitrik oksit (NO), asimetrik dimetilarjinin (ADMA) düzeyleri ile süperoksit düsmutaz (SOD) ve katalaz (CAT) aktivite değerleri ölçüldü. Bulgular: Deney grupları arasında CAT, SOD, MDA, ADMA ve NO değerleri istatistiksel olarak farklı idi (p<0,001). Post-hoc ikişerli karşılaştırma test sonuçlarına göre yalnız DEX grubu ve kontrol grubu arasında hiçbir parametrede istatistiksel fark yoktu (p>0,05). CO grubunda CAT, SOD ve NO ve Bcl-2 immünsüpresif hücre düzeyleri kontrol grubuna göre azaldı (tamamında p<0,001) ve ADMA ve MDA düzeyleri arttı (tamamında p<0,001). CO + DEX grubunda CO grubuna göre CAT, SOD ve NO düzeylerini istatistiksel olarak daha yüksekti (sırasıyla p:0,007; p:0,028; p:0,017). Sonuç: CO zehirlenmesinden yarım saat sonra uygulanan DEX CAT, SOD ve NO gibi antioksidan yapıları arttırır. Buna bağlı olarak DEX’in CO zehirlenmesi için nöroprotektif bir etkisi olabilir.

Keywords

• Deksmedetomidin
• Karbonmonoksit
• Nöroprotektif etki

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