Abstract
Objective To investigate the effects of different degrees and duration of hypothermia on severe traumatic brain injury in dogs. Methods Thirty-six one-year-old healthy dogs weighing 13-15 kg were used in this study. Traumatic brain injury model was estabhshed according to the method described by Feeney. Orthogonal design was used in this experiment. Two empirical factors: temperature (factor A) and duration (factor B) were used. Body temperature was maintained at 38 ℃ (A1), 31 ℃ (A2) or35 ℃ (A3) for 6 h (B1) or 12 h (B2).The dogs were divided into 6 groups: group A1B1 , A1B2, A2B1, A2B2, A3B1 and A3B2. Blood gas analysis was performed after the target temperature was maintained for the target duration. Neurological deficit was assessed and scored (0 = no deficit, 500 = severe neurological deficit) and blood samples were obtained at 24, 48 and 72 h after brain injury for determination of serum concentrations of neuron-specific enolase (NSE) and myelin basic protein (MBP) and plasma S-100β protein concentration. Brains were removed at the 72 h after brain injury for determination of Bcl-2 and Bax expression and detection of apoptosis in the brain. Results Hypothermia significantly decreased serum NSE, MBP and plasma S-100β concentrations, neuronal apoptosis and NDS scores;up-regulated Bcl-2 expression and down-regulated Bax expression in brain tissue in the 4 hypothermia groups (group A2B1, A2B2, A3B1 and A3B2) as compared with the control groups (group A1 B1, A1 B2). Best neuroprotective effects were observed in group A3 B1 (35 ℃ for 6 h) in terms of serum NSE, NBP and plasma S-100β concentrations, neuronal apoptosis and cerebral Bax and Bcl-2 expression, but there was no significant difference in the NDS scores among the 4 hypothermia groups. Conclusion Hypothermia can provide neuroprotection in a dog model of traumatic brain injury but the neuroprotective effect is independent of the degree and duration of hypothermia. Key words: Hypothermia, induced; Brain injuries
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