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目的观察大鼠实验性脑出血后皮层运动诱发电位(motorevokedpotential,MEP)和脊髓前角运动神经元中缝隙连接蛋白Cx32的改变。以了解脑出血后肌痉挛发生过程中脊髓运动神经元缝隙连接(gapjunction,GJ)对肌痉挛的影响。方法采用大鼠自体血缓慢注入右侧内囊后肢制备大鼠脑内囊出血致肌痉挛模型,应用电生理学方法检测皮层运动诱发电位,应用免疫组化方法观察脊髓前角运动神经元连接蛋白Cx32的改变。结果大鼠右侧内囊出血后右侧MEP波幅较左侧显著降低(P<0.01),出血1周以后病灶侧MEP波幅较出血前均显著降低(P<0.01);MEP潜伏时右侧显著延长,与左侧比较差异非常显著(P<0.01),内囊出血1周以后,MEP潜伏时均明显延长,与出血前比较差异显著(P<0.01)。脑出血后第1周,左侧脊髓灰质前角缝隙连接蛋白Cx32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,一定程度上反映了脊髓束的损伤情况和功能状态,与此同时使脊髓前角运动神经元缝隙连接数量增多,导致神经元兴奋性的同步作用增强,这可能是肌痉挛产生的重要原因。
Objective To observe the changes of Cx32 in the motoneuropathic (MEP) and anterior horn motoneurons in rats after experimental intracerebral hemorrhage. In order to understand the effect of gapjunction (GJ) of spinal motor neurons on muscle spasm during the occurrence of cerebral hemorrhage. Methods The models of intracerebral hemorrhage caused by cystic hemorrhage were prepared by slowly injecting the autologous blood of rats into the posterior limb of the hind limbs. The electrophysiologic method was used to detect the motor evoked potentials. The expressions of connexin Cx32 Change. Results The amplitude of MEP in the right side of the right posterior capsule was significantly lower than that of the left side in the right side of the rats (P <0.01), and the amplitude of MEP in the lesion side was significantly lower than that before the hemorrhage (P <0.01) (P <0.01). After 1 week of internal capsule hemorrhage, the latency of MEP prolonged significantly, which was significantly different from that before hemorrhage (P <0.01). In the first week after intracerebral hemorrhage, the connexin Cx32 in the left anterior horn of the gray matter of the left hemisphere was significantly increased, while the state of muscle spasms in the animal was significantly aggravated. Conclusions The intracapsular-oriented intracerebral hemorrhage model significantly reduces the amplitude of MEP in the lesion side of the internal capsule and prolongs the latency, which partly reflects the injury and functional status of the spinal cord bundle, and at the same time increases the number of gap junction in the anterior horn motor neurons , Resulting in the synchronization of neuronal excitability enhanced, which may be an important cause of muscle spasm.