杏仁核在腦梗死合并心律失常中的作用

賈淑偉 王玲 焦?jié)櫳?/p>

[摘要] 目的 探討杏仁核在腦梗死合并心律失常中的作用及可能機制。 方法 為觀察腦梗死后杏仁核神經(jīng)元活動的變化，將48只大鼠隨機平均分為假手術(shù)組，腦梗死后30 min、1 h、2 h、4 h和8 h組。為觀察谷氨酸在腦梗死誘發(fā)心律失常中的作用，另取40只大鼠隨機平均分為空白對照組、生理鹽水組、L-谷氨酸組、MK-801預(yù)處理后側(cè)腦室注射L-谷氨酸組和MK-801預(yù)處理后再進行中動脈栓塞（MCAO）組。通過大鼠大腦MCAO建立腦梗死模型，用生物信號采集系統(tǒng)采集心電圖，用Fos蛋白作為神經(jīng)元激活標(biāo)志物。 結(jié)果 假手術(shù)組心律失常的發(fā)生率為0，腦梗死組心律失常的發(fā)生率為78.75%，明顯高于假手術(shù)組（P < 0.01），且在心律失常發(fā)生的相應(yīng)時間點杏仁核Fos蛋白表達明顯增加（P < 0.01）。空白對照組和生理鹽水組心律失常的發(fā)生率均為0，L-谷氨酸組心律失常的發(fā)生率為87.5%，明顯高于空白對照組（P < 0.01），且L-谷氨酸組杏仁核Fos蛋白表達明顯增高（P < 0.05）。MK-801預(yù)處理后MCAO組和MK-801預(yù)處理后側(cè)腦室注射L-谷氨酸組心律失常的發(fā)生率均為0，且杏仁核Fos蛋白表達均無明顯變化（P > 0.05）。 結(jié)論 腦梗死后杏仁核活動的增強可能參與了腦梗死后心律失常的發(fā)生發(fā)展，且此作用可能由谷氨酸激活門冬氨酸受體所介導(dǎo)。

[關(guān)鍵詞] 杏仁核；腦梗死；心律失常；谷氨酸；門冬氨酸受體

[中圖分類號] R33 [文獻標(biāo)識碼] A [文章編號] 1673-7210（2018）03（a）-0020-04

[Abstract] 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 activity 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 0， 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 increased significantly during the arrhythmia （P < 0.01）. 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 incidence 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.

[Key words] Amygdala； Ischemic stroke； Arrhythmia； Glutamate； NMDA receptor

腦梗死合并心律失常是腦梗死猝死的主要原因之一[1]，其起病急、變化快的特點不能用腦疝解釋[2]，且許多腦梗死合并心律失常的患者不存在原發(fā)心臟病史[3]，提示腦梗死后心律失常的發(fā)生源于中樞神經(jīng)系統(tǒng)的活動異常。杏仁核是前腦內(nèi)參與自主神經(jīng)系統(tǒng)和心血管功能活動的重要整合中樞之一[4]。杏仁核受損時，心電圖可發(fā)生明顯改變[5]，通過刺激杏仁核可建立交感源性心律失常動物模型[6]。是否腦梗死后心律失常的發(fā)生與杏仁核的活動增強有關(guān)？本研究觀察了腦梗死后大鼠杏仁核神經(jīng)元活動的改變，并探討了其與腦梗死后心律失常發(fā)生的相關(guān)性及可能的谷氨酸能機制，以期揭示腦梗死合并心律失常的部分中樞機制。……