Abstract
Secondary traumatic brain injury is a potentially modifiable and important determinator of the outcome. Sedation and analgesia are common components of the therapy. However current drug therapies have disadvantages like respiratory depression. The objective of this study was to investigate the effect of dexmedetomidine (Dex), a sedative drug with little to no depressive effect on respiratory centers, on secondary injury in rat brain tissue. Eighteen rats were randomized into three groups: Trauma group received anesthesia, followed by head trauma with Mild Traumatic Brain Injury Apparatus, the Trauma+Dex group received additional treatment of 100µg/kg intraperitoneal dexmedetomidine daily for three days, The Control group received anesthesia only. Malondialdehyde (MDA), glutathione (GSH), Na+, K+-ATPase, or sodium/potassium (Na/K-ATPase), and cysteine-aspartic proteases, cysteine aspartates-3 (caspase-3) levels were measured. MDA levels were highest in the Trauma group (p = 0.002 vs Control group). Mean levels in the Trauma+Dex group were lower, albeit still significantly high compared to the Control group (p = 0.002). Glutathione levels were similar in all groups (p = 0.99). Na/K-ATPase levels were lowest in the Trauma group, which is significant compared to the Control group (p = 0.002) and the Trauma+Dex group (p = 0.026). Histopathologic findings of tissue degeneration like edema, vascular congestion and neuronal injury, and cleaved caspase-3 levels were lower in the Trauma+Dex group compared with the Trauma group. Dexmedetomidine administered during the early stage of traumatic brain injury may inhibit caspase-3 cleavage. However, the mechanism does not seem to be related to the improvement of MDA or GSH levels.
The Effects of Dexmedetomidine on Trauma-Induced Secondary Injury in Rat Brain
