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目的:观察大鼠脑出血后脊髓运动神经无缝隙连接(gap junction,GJ)对肌痉挛的影响。方法:采用自体血脑内注入法制备大鼠内囊出血致肌痉挛模型,检测皮质运动诱发电位(Motor Evoked Potential,MEP),应用免疫组化方法观察脊髓前角运动神经元连接蛋白C_x32的改变。结果:大鼠内囊出血后病灶侧MEP波幅较对侧显著降低(P<0.01),且出血后1周病灶侧波幅较出血前显著降低(P<0.01);MEP潜伏期显著延长(P<0.01)。脑出血后第1周,左侧脊髓灰质前角GJ蛋白C_x32显著升高,同时动物肌痉挛状态明显加重。结论:内囊定向的脑出血模型引起内囊损伤侧MEP波幅明显降低、潜伏时延长,脊髓前角运动神经元GJ数量增多。
Objective: To observe the effect of gap junction (GJ) on the spasm in the spinal cord after intracerebral hemorrhage in rats. Methods: The model of muscle spasm induced by the intracerebral hemorrhage in rats was established by autologous blood brain injection. Motor Evoked Potential (MEP) was measured. The changes of connexin C_x32 in anterior horn of spinal cord were observed by immunohistochemistry . Results: The amplitude of MEP in lesion side was significantly lower than that in the contralateral side (P <0.01), and the amplitude of lesion side was significantly lower than that in the first week after hemorrhage (P <0.01) ). In the first week after intracerebral hemorrhage, GJ protein C_x32 on the left side of the gray matter of the left hemisphere increased significantly, meanwhile, the state of muscle spasms in the animal was significantly aggravated. CONCLUSION: The intracranial-directed intracerebral hemorrhage model significantly reduces the amplitude of MEP in the lesioned side of the internal capsule, prolongs the latency and increases the number of GJ in the anterior horn of spinal cord.