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目的微血管基底膜是血脑屏障的重要组成部分,当脑缺血后,其结构将遭到损害。本研究探讨体温增加对局灶性脑缺血后,脑梗死体积及微血管的影响。方法采用大鼠大脑中动脉栓塞模型(MCAO),将模型成功大鼠随机分为对照组(37℃)和高温组(39℃),并在术后24h进行神经功能、脑梗死体积及梗死区微血管基底膜胶原蛋白Ⅳ及层粘连蛋白数量测定。结果MCAO术后24h,对照组神经功能评分为1.2±0.8,高温组2.7±0.5(P<0.01);对照组中,梗死灶体积占对侧脑体积32.5%±8.2%。高温组中,梗死灶体积占对侧脑体积百分比增加至56.1%±8.4%(P<0.01)。术后6h及24h,高温组中单位面积胶原蛋白Ⅳ与层粘连蛋白数量较对照组均下降(P<0.05)。结论脑梗死后体温升高可加重脑微血管破坏,增加脑梗死灶体积,从而加重神经功能损伤。
The purpose of microvascular basement membrane is an important part of the blood-brain barrier, when the brain ischemia, its structure will be compromised. This study explored the effect of increased body temperature on the volume of cerebral infarction and microvascular after focal cerebral ischemia. Methods Rat model of middle cerebral artery occlusion (MCAO) was used. The rats were randomly divided into control group (37 ℃) and high temperature group (39 ℃), and neurological function, infarct volume and infarct size Microvascular basement membrane collagen Ⅳ and laminin quantity determination. Results The scores of neurological function in the control group were 1.2 ± 0.8 and 2.7 ± 0.5 in the control group (P <0.01) 24 h after MCAO. In the control group, infarct size accounted for 32.5% ± 8.2% of contralateral brain volume. In the hyperthermia group, infarct volume accounted for 56.1% ± 8.4% of contralateral brain volume (P <0.01). At 6h and 24h after operation, the number of collagen Ⅳ and laminin per unit area in the high temperature group were significantly lower than those in the control group (P <0.05). Conclusion Increased body temperature after cerebral infarction may aggravate the destruction of cerebral microvascular and increase the volume of cerebral infarction, thus aggravating neurological impairment.