Abstract:OBJECTIVE: To study the neuroprotection of mild hypothermia on hypoxic ischemic brain damage (HIBD). METHODS: The HIBD model rats were randomly assigned into the 31℃ and 34℃ mild hypothermia groups, sham operated group and control group. The number of cortical neuron specific endolase (NSE) positive neurons was assayed using immunohistochemistry and the blood glucose level was detected in the four groups. RESULTS: The number of the cortical NSE positive neurons 12 and 24 h after hypoxic ischemia [( 54.3 ± 6.5 ) and ( 34.6 ± 5.6 ), respectively] in the 31℃ mild hypothermia group was significantly lower compared with the control group [( 82.3 ± 6.0 ) and ( 53.3 ± 5.6 ), respectively] (P< 0.01 or 0.05 ). It was also significantly lower in the 34℃ mild hypothermia group at 12 and 24 h [( 56.8 ± 7.1 ) and ( 32.9 ± 4.9 , respectively] compared with the control group (P< 0.01 or 0.05 ). The blood glucose level 12 and 24 h after hypoxic ischemia [( 5.74 ± 1.52 ), ( 5.89 ± 1.62 ) mmol/L, respectively] in the 31℃ mild hypothermia group was significantly higher than that in the control group [( 3.64 ± 1.22 ) and ( 4.16 ± 1.54 ) mmol/L, respectively] (both P< 0.01 ); and so was the 34℃ mild hypothermia group at 12 and 24 h [( 5.69 ± 1.48 ) mmol/L vs ( 3.64 ± 1.22 ) mmol/L; ( 5.91 ± 1.53 ) mmol/L vs ( 4.16 ± 1.54 ) mmol/L] (both P< 0.01 ). No significant difference was found in the number of cortical NSE positive neurons and blood glucose level between the 31℃ and 34℃ mild hypothermia groups. CONCLUSIONS: Mild hypothermia may have a protective effect on hypoxic ischemic neurons by restraining the NSE activity in cortical neurons and increasing the blood glucose level.
