Comparison of effects of dexmedetomidine and magnesium in traumatic brain injury; [Travmatik beyin hasarinda serebral korumada deksmedetomidin ve magnezyumun etkilerinin karşilaştirilmasi]
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2006
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Aim: Prevention of secondary serebral injury plays a major role in intensive care of head injury patients. In this study, the effects of dexmedetomidine and magnesium to prevent brain injury in head trauma are compared. Materials and Methods: Diffuse head injury was induced in 30 adult Wistar albino male rats by Marmarou method after anesthetized by intraperitoneal injection of 30 mg kg-1 sodium thiopental. Rats were divided randomly into 3 groups, each consisting of 10 rats: 2 mL saline to Group 1, 2 mL 100 μg kg-1 dexmedetomidine to Group II and 2 mL 750 μmol kg-1 magnesium sulphate to Group III were administered by intraperitoneal route. Rats were sacrificed by cervical dislocation 120 minutes after the drug administration and brain tissues were obtained without damaging the brains. Brain tissue samples were divided into two by interhemispheric incision for biochemical and histological analysis. Brain tissues were fixed in 10% formalin solution and embedded in paraffin and examined by hematoxylin-eosin staining for morphological alterations. Sections were stained via TUNEL method in order to detect apoptosis. The tissue concentration of malonyldialdehyde (MDA), Superoxide dismutase (SOD) and glutathione peroxidasc (GSH-Px) in brain tissue was also measured. Results: Hematoxylin-eosin-stained brain sections arc compared; dexmedetomidine is more effective than magnesium in reducing brain cell injury caused by head trauma. Evaluation of apoptosis by the TUNEL method revealed that magnesium is more effective than dexmedetomidine in preventing cell death. Malonyldialdehyde (MDA) levels of Group I was found significantly lower than Group II and III (p<0.05). Also the decrease in the level of superoxide dismutase (SOD) in Group I was found significantly higher than Group II and III. There was no difference in glutathione peroxidasc (GSH-Px) levels between the groups. Conclusion: Dexmedetomidine reduces secondary cerebral injury significantly: however, magnesium prevents apoptosis more effective than dexmedetomidine in experimental models of diffuse traumatic brain injury. The effects of magnesium and dexmedetomidine in brain cell protection may occur through different mechanisms but not by enzymes because the biochemical results arc in contradiction with the histopathological analysis.