The effects of dexmedetomidine on trauma-induced secondary injury in rat brain

Abstract

ABSTRACTBackgroundThe objective of this study was to investigate the effect of dexmedetomidine (Dex), a sedative drug with little or no depressant effect on respiratory centers, on secondary injury in rat brain tissue by means of the Na+/K+ ATPase enzyme, which maintains the cell membrane ion gradient; malondialdehyde, an indicator of membrane lipid peroxidation; glutathione, an indicator of antioxidant capacity; and histopathological analyses.MethodsEighteen rats were randomized into three groups: the trauma group received anesthesia, followed by head trauma with a Mild Traumatic Brain Injury Apparatus; the Trauma+Dex group received an additional treatment of 100 µg/kg intraperitoneal dexmedetomidine daily for three days; the Control group received anesthesia only.ResultsThe highest MDA levels compared to the Control group were found in the Trauma group. Mean levels in the Trauma+Dex group were lower, albeit still significantly high compared to the Control group. Glutathione levels were similar in all groups. Na/K-ATPase levels were significantly lower in the Trauma group compared to both the Control group and the Trauma+Dex group. Histopathologic findings of tissue degeneration including edema, vascular congestion and neuronal injury, and cleaved caspase-3 levels were lower in the Trauma+Dex group compared with the Trauma group.ConclusionsDexmedetomidine administered during the early stage of traumatic brain injury may inhibit caspase-3 cleavageHowever, the mechanism does not seem to be related to the improvement of MDA or GSH levels.