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目的 探讨低温干预起始时间对新生大鼠缺氧缺血性脑损伤的影响。方法 Wistar 7日龄新生大鼠,随机分到:缺氧缺血后0 min、60 min、120 min、6 h起始亚低温干预组、常温(37℃)恢复组、正常对照组(假结扎组),每组30只。每组20只于缺氧缺血后78 h处死,10只用于测定脑组织含水量,10只经灌注固定,冠状切片进行微管相关蛋白-2(MAP-2)免疫组化染色,测定脑梗塞面积;另外10只于生后42d用迷宫实验检测其学习和记忆能力。结果 (1)亚低温干预各组大鼠脑组织含水量与常温恢复组相比显著减少(P<0.05);(2)亚低温干预各组大鼠脑梗塞面积与常温恢复组相比显著降低(P<0.05),且随着亚低温干预起始时间的延迟,梗塞面积逐渐增大;延迟6 h的干预仍有效;(3)亚低温干预各组大鼠学习和记忆能力显著高于常温恢复组(P<0.05)。结论亚低温干预效果与缺氧缺血后低温的起始时间有关,延迟6 h的亚低温干预仍有效。
Objective To investigate the effect of hypothermia intervention on hypoxic-ischemic brain damage in neonatal rats. Methods Wistar 7-day-old neonatal rats were randomly divided into four groups: initial hypothermia intervention group (0 min, 60 min, 120 min, 6 h after hypoxia / ischemia), normal temperature (37 ℃) Group), 30 in each group. Twenty rabbits were sacrificed at 78 h after hypoxia-ischemia, 10 were used to determine the water content of brain tissue, 10 were fixed by perfusion and coronarial sections were used for the immunohistochemical staining of MAP-2. Cerebral infarction area; the other 10 only after 42 days of life with maze test to test its learning and memory ability. Results (1) Compared with normal temperature recovery group, the water content of brain tissue of rats in mild hypothermia intervention group decreased significantly (P <0.05); (2) Compared with normal temperature recovery group, (P <0.05). And with the delay of onset time of mild hypothermia, infarction area gradually increased; 6 h delay was still effective; (3) The learning and memory ability of rats in mild hypothermia intervention group was significantly higher than that of normal temperature Recovery group (P <0.05). Conclusion The effect of mild hypothermia is related to the onset time of hypothermia after hypoxia-ischemia, and the mild hypothermia intervention delayed 6 h is still effective.