|
|
|
| Involvement of the Amygdala in the cerebral infarction complicated with arrhythmias |
| JIA Shuwei WANG Ling JIAO Runsheng |
| Department of Physiology, Harbin Medical University, Heilongjiang Province, Harbin 150086, China |
|
|
|
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.
|
|
|
|
|
|
[1] Wira CR，Rivers E，Martinez-Capolino C，et al. Cardiac complications in acute ischemic stroke [J]. West J Emerg Med，2011，12（4）：414-420.
[2] 杨贤义，刘梅，朱艳霞，等.急诊室成功抢救脑心综合征致猝死11例分析[J].中西医结合心脑血管病杂志，2012， 10（1）：123-124.
[3] Dogan A，Tunc E，Ozturk M，et al. Electrocardiographic changes in patients with ischaemic stroke and their prognostic importance [J]. Int J Clin Pract，2004，58（5）：436-440.
[4] Takeuchi Y，Xie Q，Miki T，et al. Parabrachial inputs to Fos-immunoreactive neurons in the lateral central nucleus of amygdala activated by hypotension： a light and electron microscopic study in the rat [J]. Brain Res Bull，2004，64（2）：171-180.
[5] 任建刚.脑心综合征的中西医机制研究探析[J].中外医疗，2011，30（35）：118.
[6] 蒋萌，朱思明，袁孝如.中枢性心律失常时心肌收缩力变化的实验研究[J].心功能杂志，1995，7（1）：8-12.
[7] 贾淑伟，王玲，焦润生.延髓头端腹外侧部在脑梗死合并心律失常中的作用[J].中国医药导报，2016，13（31）：11-15.
[8] 贾淑伟，夏青.线栓法建立局灶性脑缺血模型的方法与探讨[J].中国医药导报，2014，11（24）：33-35.
[9] Jia SW，Xia Q，Zhang BP，et al. Involvement of the paraventricular nucleus in the occurrence of arrhythmias in middle cerebral artery occlusion rats [J]. J Stroke Cerebrovas Dis，2015，24（4）：844-851.
[10] Sun L，Ai J，Wang N，et al. Cerebral Ischemia Elicits Aberration in Myocardium Contractile Function and Intracellular Calcium Handling [J]. Cell Physiol Biochem，2010，26（3）：421-430
[11] Ji H，Wang L，Bi H，et al. Mechanisms of lumbrokinase in protection of cerebral ischemia [J]. Eur J Pharmacol，2008，590（1-3）：281-289.
[12] Colivicchi F，Bassi A，Santini M，et al. Prognostic implications of right-sided insular damage，cardiac autonomic derangementand arrhythmias after acute ischemic stroke [J]. Stroke，2005，36（8）：1710-1715.
[13] Sörös P，Hachinski V.Cardiovascular and neurological causes of sudden death after ischaemicstroke [J]. Lancet Neurol，2012，11（2）：179-188.
[14] Walker JE，FonnumF. Regional cortical glutamergic and aspartergic projections to the amygdala and thalamus of the rat [J]. Brain Res，1983，267（2）：371-374.
[15] 欧阳明，王绍.中央杏仁核内微量注射地塞米松对NA／NPY在NTS所致心血管救应的影响[J].中国兽医学报，1999，19（6）：584-587.
[16] Dunn AJ，Swiergiel AH，Palamarchouk V. Brain circuits involved in corticotropin-releasing factor-norepinephrine interactions during stress [J]. Ann N Y Acad Sci，2004， 1018：25-34.
[17] Veening JG，Swanson LW，Sawchenko PE. The organization of projections from the central nucleus of the amygdala to brainstem sites involved in central autonomic regulation：a combined retrograde transport-immunohistochemical study [J]. Brain Res，1984，303（2）：337-357.
[18] 顾蕴辉，徐伟科，吕贻春，等.中央杏仁核、外侧下丘脑/穹窿周围区、室旁核均参与岛皮层升压反应[J].生理学报，1997，49（2）：221-226.
[19] Yang MX，Yu WT，Hu JK，et al. Effect of Zhongfengkang on cerebral glutamate and calcium of rats with focal cerebral ischemia [J]. Chinese Journal of integrative medicine on cardio/cerebrovascular disease，2005，3（10）：877-878.
[20] 党连生，徐燕，王晓霞，等.谷氨酸与缺血性脑卒中早期进展关系的研究[J].中华老年心脑血管病杂志，2013， 15（1）：57-59.
|
|
|
|
