Issue release date: 12.11.2024
2Kirikkale University, Faculty of Medicine, Department of Neurosurgery, Kirikkale, Turkey
3Hacettepe University, Faculty of Medicine, Department of Histology and Embryology, Ankara, Turkey
4Hacettepe University, Faculty of Medicine, Department of Biochemistry, Ankara, Turkey DOI : 10.5137/1019-5149.JTN.6757-12.0 AIM: To compare the effect of dexmedetomidine administered by intracisternal route with by intravenous route on brain tissue of rat after incomplete cerebral ischemia.
MATERIAL and METHODS: Cerebral ischemia was produced by the combination of right common carotid artery occlusion and hemorrhagic hypotension during 30 minutes. Thirty minutes before the ischemia, 0.1 ml 0.9% NaCl (Group SIC, n=6) or 9 μg/kg dexmedetomidine (Group DIC, n=6) was administered into the cisterna magna. For the intravenous groups, 9 μg/kg dexmedetomidine (Group DIV, n=6) or 0.9% NaCl (Group CONTROL, n=6) 5 ml/kg/h was given in 2 hours. After 24 hours, the lipid peroxidation levels were measured in the brain tissue and plasma. Hippocampal formations were used for histopathological examination.
RESULTS: Intravenous dexmedetomidine produced a decrease in baseline mean arterial blood pressure and plasma glucose concentrations. There was a significant difference between the DIV group and DIC, SIC, CONTROL groups regarding the brain lipid peroxidation levels (p<0.001, p<0.001, p=0.001, respectively), and regarding the picnotic neuronal cell count (p<0.001, p=0.01, p=0.009, respectively). Mean plasma lipid peroxidation levels of the DIV group was different from the DIC group (p=0.003).
CONCLUSION: Systemically administered dexmedetomidine had neuroprotective effect in ischemia-induced neuronal damage, but centrally administered dexmedetomidine did not.
Keywords : Dexmedetomidine, Intracisternal, Intravenous, Ischemia, Brain injury