杏仁核在脑梗死合并心律失常中的作用

Involvement of the Amygdala in the cerebral infarction complicated with arrhythmias

目的探讨杏仁核在脑梗死合并心律失常中的作用及可能机制。方法为观察脑梗死后杏仁核神经元活动的变化,将48只大鼠随机平均分为假手术组,脑梗死后30 min、1 h、2 h、4 h和8 h组。为观察谷氨酸在脑梗死诱发心律失常中的作用,另取40只大鼠随机平均分为空白对照组、生理盐水组、L-谷氨酸组、MK-801预处理后侧脑室注射L-谷氨酸组和MK-801预处理后再进行中动脉栓塞(MCAO)组。通过大鼠大脑MCAO建立脑梗死模型,用生物信号采集系统采集心电图,用Fos蛋白作为神经元激活标志物。结果假手术组心律失常的发生率为0,脑梗死组心律失常的发生率为78.75%,明显高于假手术组(P<0.01),且在心律失常发生的相应时间点杏仁核Fos蛋白表达明显增加(P<0.01)。空白对照组和生理盐水组心律失常的发生率均为0,L-谷氨酸组心律失常的发生率为87.5%,明显高于空白对照组(P<0.01),且L-谷氨酸组杏仁核Fos蛋白表达明显增高(P<0.05)。MK-801预处理后MCAO组和MK-801预处理后侧脑室注射L-谷氨酸组心律失常的发生率均为0,且杏仁核Fos蛋白表达均无明显变化(P>0.05)。结论脑梗死后杏仁核活动的增强可能参与了脑梗死后心律失常的发生发展,且此作用可能由谷氨酸激活门冬氨酸受体所介导。

Objective To investigate the association between ischemic stroke-induced arrhythmia and the activity of amygdala and the possible mechanism. Methods Forty-eight rats were randomly and equally divided into the following groups： sham-operated group, 30 min, 1 h, 2 h, 4 h, and 8 h after ischemic stroke groups, and the changes of the ac- tivity of amygdala neurons in ischemic stroke rats were observed. Forty rats were randomly and equally divided into the following groups： blank control group, saline group, L-glutamate group, MK-801 before L-glutamate and MK-801 preceding making model group, and the effects of glutamate on arrhythmia induced by ischemic stroke were observed. The experimental cerebral ischemic animal model was established by occluding the right middle cerebral artery （MCAO）. The electrocardiography was recorded by a biological signal collecting and processing system. Fos protein was used as an objective indicator to illustrate the functional state of neurons. Results The incidence of arrhythmia in model group was O, and the sham-operated group was 78.75%, the incidence of arrhythmia in the sham-operated group was significantly higher than that in model group （P 〈 0.01）, and the expression of Fos protein in the amygdala was also in- creased significantly during the arrhythmia （P 〈 0.0l）. The incidence of arrhythmia in blank control group and saline group was 0, L-glutamate group was 87.5%, which was significantly higher than blank control group （P 〈 0.01）, and the expression of Fos protein in the amygdala of the L-glutamate group was also increased significantly （P 〈 0.05）. The inci- dence of arrhythmia in both MK-801 preceding making model group and MK-801 preceding L-glutamate group was 0, and the expression of Fos protein had no obvious change （P 〉 0.05）. Conclusion It is concluded that activation of the amygdala in ischemic stroke rats is likely mediated by glutamate via activation of N-methyl-D-aspartic acid receptors, which causes arrhythmias.