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目的:研究全脑缺血后30min开始的低温对沙土鼠行为学和组织病理学的影响,并与脑缺血后即刻低温进行比较。方法:采用沙土鼠全脑缺血模型,缺血时间10min。动物随机分为4组:假手术组、常温组、延迟性低温组和即刻低温组,每组7只。于脑缺血后第5天行开阔法行为学检查,第7天行海马CA1区组织病理学检查。结果:常温组10min爬过的格子数(651±108)较假手术组(278±67)、延迟性低温组(478±89)、即刻低温组(368±46)有明显增多(t=7.76,2.21,6.37,P<0.0d 1～0.05)。延迟性低温组较假手术组和即刻低温组增多(t=4.75,2.90,P<0.01～0.05)。海马CA1区内侧神经元数(以正常海马成活神经元的百分数表示,即各组成活神经元数与假手术组之比):延迟性低温组(42±7)%较常温缺血组(5±1)%多(t=13.00,P<0.01),不及即刻低温组(66±10)%(t=5.20,P<0.01)。海马CA1区中间神经元计数:延迟性低温组(60±9)%较常温缺血组(10±4)%多(t=13.20,P<0.01),不及即刻低温组(77±16)%多(t=2.45,P<0.05)。海马CA1区外侧成活神经元计数:延迟性低温(71±13)%和即刻低温组(80±14)%之间无差别(t=1.25,P>0.05),均较常温组(23±5)%多(t=9.14,t=10.14,P均<0.01)。结论:延迟性低温可以减轻全脑缺血后神经功能障碍和海马神经元坏死,但作用不及即刻低温。
OBJECTIVE: To study the effects of hypothermia beginning 30 min after global ischemia on behavior and histopathology of gerbils and to compare them with the hypothermia immediately after cerebral ischemia. Methods: The gerbil model of cerebral ischemia was used. The ischemic time was 10 min. The animals were randomly divided into 4 groups: sham operation group, normal temperature group, delayed hypothermia group and immediate hypothermia group, 7 rats in each group. Behavioral examination was performed on the fifth day after cerebral ischemia, and histopathological examination of hippocampal CA1 area was performed on the 7th day. Results: The number of grids climbed at 10min in normal temperature group was significantly higher than that in sham operation group (278 ± 67), delayed hypothermia group (478 ± 89) and immediate hypothermia group (368 ± 46) (t = 7.76 , 2.21, 6.37, P <0.0d 1 ~ 0.05). Delayed hypothermia group than the sham operation group and immediate hypothermia group increased (t = 4.75,2.90, P <0.01 ~ 0.05). The number of neurons in the hippocampal CA1 region (expressed as a percentage of normal hippocampal neurons, that is, the ratio of the number of viable neurons in each group to the sham group): delayed hypothermic group (42 ± 7)% compared with warm ischemia group (T = 13.00, P <0.01), which was lower than that of immediate hypothermia group (66 ± 10)% (t = 5.20, P <0.01). The number of interneurons in the hippocampal CA1 region was significantly lower than that of the immediate hypothermia group (60 ± 9% vs 10 ± 4%, t = 13.20, P <0.01) More (t = 2.45, P <0.05). Surviving neurons outside the hippocampal CA1 region were significantly higher than those in the normothermia group (23 ± 5 vs. 71 ± 13% vs 80 ± 14%, t = 1.25, P> 0.05) )% (T = 9.14, t = 10.14, P <0.01). Conclusion: Delayed hypothermia can reduce neurological deficit and neuronal necrosis after global cerebral ischemia, but the effect is less than immediate hypothermia.