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目的 :探讨大剂量甲基强地松龙对慢性脑血管痉挛的作用机制。方法 :将成年犬随机分成大剂量甲基强地松龙 (MP ,10mg/kg)治疗组和对照组 ,治疗组和对照组又根据犬脑血管痉挛动态发展过程中不同阶段各分为A ,B ,C ,D 4个小组。通过枕大池二次注血法建立犬脑血管痉挛模型 ,经脑血管造影观察犬脑血管痉挛的动态发展过程。应用酶联免疫生化技术检测各组犬基底动脉血管平滑肌细胞胞膜蛋白激酶C(PKC)活性。应用体外血管张力性研究方法观察PKC激活剂 (phorobol12 myristate 13 acetate ,PMA)和高钾溶液对血管张力的影响 ,及甲基强地松龙对PMA和高钾溶液引起的血管张力的影响。结果 :经脑血管造影证实该剂量甲基强地松龙明显减轻了实验性脑血管痉挛的严重程度 ,与对照组相比 ,PKC活性在大剂量甲基强地松龙治疗组没有明显增高。体外血管张力性研究显示甲基强地松龙没有影响高钾引起的血管张力变化 ,相反 ,却明显抑制了PKC的激活剂PMA引起的血管张力性收缩。结论 :大剂量甲基强地松龙能够明显减轻脑血管痉挛程度 ,这种作用是通过抑制血管平滑肌细胞PKC活性 ,而不是作为Ca2 + 拮抗剂来发挥防治脑血管痉挛的发生发展
Objective: To investigate the mechanism of high dose methylprednisolone on chronic cerebral vasospasm. Methods: Adult dogs were randomly divided into high dose methylprednisolone (MP, 10mg / kg) treatment group and control group. The treatment group and control group were divided into three groups according to the stages of dynamic development of canine cerebral vasospasm: A, B, C, D 4 groups. The dog model of cerebral vasospasm was established by the secondary injection of occipital cistern, and the dynamic development of canine vasospasm was observed by cerebrovascular angiography. Enzyme-linked immunosorbent assay (ELISA) was used to detect the membrane protein kinase C (PKC) activity in basilar artery smooth muscle cells of dogs. The effect of PKC activators (phorobol 12 myristate 13 acetate, PMA) and high potassium on vascular tone and the effect of methylprednisolone on the vascular tone induced by PMA and potassium solution were observed by in vitro vascular tension study. Results: Cerebral angiography confirmed that this dose of methylprednisolone significantly reduced the severity of experimental cerebral vasospasm. Compared with the control group, PKC activity was not significantly increased in the high-dose methylprednisolone treatment group. In vitro vascular tension studies have shown that methylprednisolone did not affect the vascular tension caused by high potassium, on the contrary, but significantly inhibited PKC activator of PMA-induced vasoconstriction. Conclusion: High-dose methylprednisolone can significantly reduce the degree of cerebral vasospasm, which can prevent and treat the development of cerebral vasospasm by inhibiting the PKC activity of vascular smooth muscle cells instead of acting as Ca2 + antagonist