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目的探讨大面积脑梗塞超早期开始使用盐酸法舒地尔的效果,动态监测血清S100β蛋白,初步评价其药效,探讨其作用机制,为更好地指导临床用药提供实验学证据。方法运用介入技术及自体血栓栓塞建立家兔大脑中动脉梗塞模型,术后随机分成生理盐水组和盐酸法舒地尔组。盐酸法舒地尔组每日静脉给予盐酸法舒地尔9mg/kg,并每隔24h检测一次血清S100β蛋白及神经功能缺损评分,7d后处死家兔后行脑组织切片,TTC染色后计算梗塞体积大小。结果造模后7d,两组家兔均存活;盐酸法舒地尔组家兔半球梗塞体积明显小于生理盐水组(P<0.01);盐酸法舒地尔组神经功能评分普遍优于生理盐水组。盐酸法舒地尔组较盐水对照组血清S100β蛋白浓度低,且出现浓度高峰延迟。结论急性大面积脑梗塞超早期(6h)开始使用盐酸法舒地尔7d后能明显缩小梗塞面积,明显改善预后,其作用之一可能归功于抑制炎症反应、促进神经修复,在治疗急性大面积脑梗塞时值得临床进一步推广。
Objective To investigate the effect of early onset of large-area cerebral infarction with fasudil hydrochloride and to monitor the serum S100β protein dynamically to evaluate its efficacy and to explore its mechanism of action to provide experimental evidence for better guidance of clinical drug use. Methods The middle cerebral artery occlusion model of rabbits was established by interventional technique and autologous thromboembolism. The rabbits were randomly divided into normal saline group and fasudil hydrochloride group. Fasudil hydrochloride group was given daily intravenous fasudil hydrochloride 9mg / kg. Serum S100β protein and neurological deficit score were measured every 24h. After 7 days, the rabbits were sacrificed and brain slices were obtained. TTC staining was used to calculate infarction Size Results Rabbits in both groups survived 7 days after modeling. The volume of hemispheric infarction in fasudil hydrochloride group was significantly lower than that in saline group (P <0.01). The neurological score of Fasudil hydrochloride group was generally better than that of saline group . Serum S100β protein concentration in fasudil hydrochloride group was lower than that in saline control group, and the peak concentration was delayed. Conclusion Acute large area cerebral infarction can significantly reduce the infarct size and improve the prognosis significantly after the start of fasudil hydrochloride for 7 days in early stage (6h). One of its effects may be attributed to the inhibition of inflammatory reaction and the promotion of nerve repair. In the treatment of acute large area It is worth further clinical promotion of cerebral infarction.