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目的 :为了深入研究SAH后CVS的发生机制及其治疗效果。方法 :42只大鼠随机分 :A组 :正常对照组 ;B组 :注射 0 9%氯化钠对照组 ;C组 :采用 0 1、0 2、0 3、0 4、0 5ml自体动脉血注入大鼠枕大池制作CVS模型。观察大鼠的存活、临床表现、血压、血气分析、rCBF测定及病理学检查等。结果 :B组大鼠均存活 ,临床表现典型及和病理学改变轻微 ,与A组差异不明显。C4 :大鼠均存活 ,但反应迟钝 ,自洁性差 ,血压短暂升高 ,rCBF下降明显 ,持续时间长 ;颅底出血 ,颅底动脉管壁破坏、层次结构消失 ,与B组差别显著。C1～ 3组大鼠死亡率高。C5组大鼠临床表现肌病理改变不明显。结论 :注射 0 2ml时 ,大鼠存活率高 ,临床表现典型 ,rCBF降低和病理改变明显 ,而且与慢性出血性脑血管痉挛相一致 ,是最理想的CVS模型。
Objective: In order to further study the mechanism of CVS after SAH and its therapeutic effect. Methods: Forty-two rats were randomly divided into group A: normal control group, group B: injection of 0.9% sodium chloride control group, group C: 0 1,0 2,0 3,0 4,0 5ml autologous arterial blood Into the rat pillow pool CVS model. Observe the survival of rats, clinical manifestations, blood pressure, blood gas analysis, rCBF determination and pathological examination. Results: All the rats in group B survived, with typical clinical manifestations and slight changes in pathology. There was no significant difference with group A. C4: Rats all survived, but they were unresponsive, poor self-cleaning, short-term rise in blood pressure, and decreased rCBF, which lasted for a long time. The skull base hemorrhage, the rupture of the skull base artery wall and the layer structure disappeared. C1 ~ 3 group of rats with high mortality. The clinical manifestations of the rats in C5 group showed no significant changes in myopathy. CONCLUSION: When 0 2 ml is injected, the survival rate of rats is high, the clinical manifestations are typical, the rCBF is reduced and the pathological changes are obvious, and consistent with chronic hemorrhagic cerebral vasospasm, which is the best CVS model.