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.
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.