交感神经放电对大鼠心室电生理影响的研究
发布时间：2018-08-08 17:57
【摘要】：目的:学习大鼠心肌梗死模型的制作,建立测量颈交感神经电活动的方法及单电极测定心室肌表面单相动作电位,以探索交感神经在大鼠心肌梗死后室性心律失常的作用及促进正常大鼠心脏表面交感神经芽生是否使大鼠更易发生心律失常。方法:麻醉状态下,气管插管,开胸并在左心耳下缘结扎大鼠冠状动脉前降支,使前壁心肌细胞急性缺血以制作心肌梗死模型。切开颈前皮肤,找到颈交感神经,剥离交感神经束外膜,并与外周肌肉及软组织隔离,连接电生理仪测定颈交感神经电活动。(1)6-羟多巴胺(6-hydroxydopamine,6-OHDA)去交感神经支配模型:大鼠随机分为假手术组(sham+Vc)、假手术对照组(sham+6-OHDA)、心肌梗死组(AMI+Vc)和心肌梗死对照组(AMI+6OHDA),sham+6-OHDA组和AMI+6OHDA组用6-羟多巴胺(6OHDA)化学性去除交感神经3天,sham+Vc和AMI+Vc予以等剂量的0.2%维生素C溶剂。在麻醉并气管插管下,监测体表心电图、颈交感神经电活动、颈动脉血压,程序刺激(Programmed Electrical Stimulation,PES)测量心室有效不应期(Ventricular Effective Refractory Period,VERP)、室性心律失常。(2)4-甲基邻苯二酚(4-methylcatechol,4-MC)促进心脏表面交感神经芽生模型。大鼠被随机分为正常组(Phosphate Buffer Solution,PBS)和实验组(4-MC),实验组予以4-MC腹腔注射30天以促进交感神经芽生,正常组予以等剂量PBS溶剂。麻醉后测量体表心电图、颈交感神经电活动、颈动脉血压、及心室表面电生理。结果:(1)AMI+Vc组RR值明显大于其他三组(P0.05),AMI+Vc组QRS波明显大于sham+Vc组和AMI+6OHDA组,AMI+Vc组QT间期明显大于sham+Vc组和AMI+6OHDA组(P0.05),而P波、PR间期、ERP在各组间无统计学差异。AMI+Vc组非梗死区APD50、APD90较sham+VC组及sham+6-OHDA组显著延长(P0.05),AMI+Vc组梗死周边区APD50、APD90较其他三组显著延长(P0.05)。各组间的APD电交替频率没有统计学差别,但心肌梗死后的频率低于非梗死组。AMI+Vc组大鼠更易诱发出室性心律失常,给予6-OHDA的大鼠均未诱导出心律失常。大鼠颈交感神经放电活动增加后可诱发室性心律失常,给予6-OHDA后未见室性心律失常的发生。心肌梗死及6-OHDA阻断交感神经后,颈动脉压没有明显统计学差别,但较sham+Vc组血压下降。(2)4MC促进心脏表面交感神经芽生,但体表心电图、心室有效不应期、颈动脉血压、诱发室性心律失常率等在两组间没有明显的统计学差异。4MC组左心肌组织APD90明显大于正常组(P0.05)。两组比较引起APD电交替的刺激频率无明显差别,但4MC组稍低于PBS组。结论:1.6-OHDA使交感神经去支配可能减少了心肌梗死后大鼠室性心律失常的发生。2.4-MC促进正常大鼠的交感神经芽生可使其左侧心室单相动作电位时程延长,但并不增加心律失常发生率。3.交感神经可能参与了病理状态下室性心律失常的发生,且阻断交感神经神经递质的释放可能会减少室性心律失常、甚至是恶性室性心律失常的发生。
[Abstract]:Objective: To study the making of rat model of myocardial infarction, to establish a method of measuring the electrical activity of the sympathetic nerve of the neck and to determine the single phase action potential of the ventricular muscle surface by single electrode in order to explore the role of sympathetic nerve in the ventricular arrhythmia after myocardial infarction in rats and to promote the more prone to heart of the normal rat's sympathetic buds. Methods: under anaesthetized state, endotracheal intubation, thoracotomy, and ligation of the anterior descending branch of the rat coronary artery at the lower edge of the left atrial appendage made acute ischemia of the anterior wall of the wall to make the myocardial infarction model. The anterior skin of the neck was cut, the cervical sympathetic nerve was found, the sympathetic fascicular outer membrane was stripped, and the peripheral muscles and soft tissues were isolated, and the electrophysiologic apparatus was connected to the electrophysiologic instrument. Electrical activity of cervical sympathetic nerve. (1) 6- hydroxydopamine (6-hydroxydopamine, 6-OHDA) denervation model: rats were randomly divided into sham operation group (sham+Vc), sham operation control group (sham+6-OHDA), myocardial infarction group (AMI+Vc) and myocardial infarction control group (AMI+6OHDA), sham+6-OHDA and AMI+6OHDA group with 6- hydroxyl dopamine (6OHDA) chemical removal 3 days of the sensory nerve, sham+Vc and AMI+Vc were given equal doses of 0.2% vitamin C solvents. Under anesthesia and tracheal intubation, the body surface electrocardiogram, cervical sympathetic electrical activity, carotid artery blood pressure, and Programmed Electrical Stimulation, PES were used to measure ventricular effective refractory period (Ventricular Effective Refractory Period, VERP) and ventricular rhythm. Abnormal. (2) 4- methyl catechol (4-methylcatechol, 4-MC) promoted the sympathetic buds model of the heart surface. Rats were randomly divided into normal group (Phosphate Buffer Solution, PBS) and experimental group (4-MC). The experimental group was given 4-MC intraperitoneal injection for 30 days to promote sympathetic buds, and the normal group was given equal dose of PBS solvent. After anesthesia, the body surface heart was measured. Electrogram, cervical sympathetic electrical activity, carotid blood pressure, and ventricular surface electrophysiology. Results: (1) the RR value of group AMI+Vc was significantly greater than that of other three groups (P0.05), QRS wave in group AMI+Vc was significantly greater than that of group sham+Vc and AMI+6OHDA group, and AMI+Vc group QT interval was obviously greater than sham+Vc group and AMI+6OHDA group (P0.05), but there was no statistical difference between each group. In group Vc, the non infarct area was APD50, APD90 was significantly longer than that in group sham+VC and sham+6-OHDA group (P0.05). APD90 in group AMI+Vc was significantly longer than that in other three groups (P0.05). The frequency of APD electrical alternation between groups was not statistically different, but the frequency of post infarction was lower than that of rats in non infarction group. The rats given 6-OHDA did not induce arrhythmia. The ventricular arrhythmia was induced by the increase of the activity of the cervical sympathetic nerve in rats. No ventricular arrhythmia occurred after 6-OHDA. After myocardial infarction and 6-OHDA blocking of sympathetic nerve, there was no significant difference between the carotid pressure and the blood pressure in the sham+Vc group. (2) 4MC promoted the heart meter. Facial sympathetic buds, but the body surface electrocardiogram, the ventricular effective refractory period, the carotid blood pressure, the induced ventricular arrhythmia rate, and so on, there was no significant difference between the two groups in the two groups. The left myocardial tissue APD90 in the group.4MC was significantly larger than the normal group (P0.05). The two groups had no significant difference in the pricking frequency of the APD electric alternation, but the 4MC group was slightly lower than the PBS group. 1.6-OHDA makes the sympathetic denervation may reduce the occurrence of ventricular arrhythmia in rats after myocardial infarction and.2.4-MC promotes the sympathetic buds of normal rats to prolong the left ventricular monophasic action potential duration, but it does not increase the incidence of arrhythmia,.3. sympathetic nerve may participate in the onset of ventricular arrhythmia in the pathological state. Blocking the release of sympathetic neurotransmitters may reduce the occurrence of ventricular arrhythmias, even malignant ventricular arrhythmias.
【学位授予单位】：皖南医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R542.22
本文编号：2172573
[Abstract]:Objective: To study the making of rat model of myocardial infarction, to establish a method of measuring the electrical activity of the sympathetic nerve of the neck and to determine the single phase action potential of the ventricular muscle surface by single electrode in order to explore the role of sympathetic nerve in the ventricular arrhythmia after myocardial infarction in rats and to promote the more prone to heart of the normal rat's sympathetic buds. Methods: under anaesthetized state, endotracheal intubation, thoracotomy, and ligation of the anterior descending branch of the rat coronary artery at the lower edge of the left atrial appendage made acute ischemia of the anterior wall of the wall to make the myocardial infarction model. The anterior skin of the neck was cut, the cervical sympathetic nerve was found, the sympathetic fascicular outer membrane was stripped, and the peripheral muscles and soft tissues were isolated, and the electrophysiologic apparatus was connected to the electrophysiologic instrument. Electrical activity of cervical sympathetic nerve. (1) 6- hydroxydopamine (6-hydroxydopamine, 6-OHDA) denervation model: rats were randomly divided into sham operation group (sham+Vc), sham operation control group (sham+6-OHDA), myocardial infarction group (AMI+Vc) and myocardial infarction control group (AMI+6OHDA), sham+6-OHDA and AMI+6OHDA group with 6- hydroxyl dopamine (6OHDA) chemical removal 3 days of the sensory nerve, sham+Vc and AMI+Vc were given equal doses of 0.2% vitamin C solvents. Under anesthesia and tracheal intubation, the body surface electrocardiogram, cervical sympathetic electrical activity, carotid artery blood pressure, and Programmed Electrical Stimulation, PES were used to measure ventricular effective refractory period (Ventricular Effective Refractory Period, VERP) and ventricular rhythm. Abnormal. (2) 4- methyl catechol (4-methylcatechol, 4-MC) promoted the sympathetic buds model of the heart surface. Rats were randomly divided into normal group (Phosphate Buffer Solution, PBS) and experimental group (4-MC). The experimental group was given 4-MC intraperitoneal injection for 30 days to promote sympathetic buds, and the normal group was given equal dose of PBS solvent. After anesthesia, the body surface heart was measured. Electrogram, cervical sympathetic electrical activity, carotid blood pressure, and ventricular surface electrophysiology. Results: (1) the RR value of group AMI+Vc was significantly greater than that of other three groups (P0.05), QRS wave in group AMI+Vc was significantly greater than that of group sham+Vc and AMI+6OHDA group, and AMI+Vc group QT interval was obviously greater than sham+Vc group and AMI+6OHDA group (P0.05), but there was no statistical difference between each group. In group Vc, the non infarct area was APD50, APD90 was significantly longer than that in group sham+VC and sham+6-OHDA group (P0.05). APD90 in group AMI+Vc was significantly longer than that in other three groups (P0.05). The frequency of APD electrical alternation between groups was not statistically different, but the frequency of post infarction was lower than that of rats in non infarction group. The rats given 6-OHDA did not induce arrhythmia. The ventricular arrhythmia was induced by the increase of the activity of the cervical sympathetic nerve in rats. No ventricular arrhythmia occurred after 6-OHDA. After myocardial infarction and 6-OHDA blocking of sympathetic nerve, there was no significant difference between the carotid pressure and the blood pressure in the sham+Vc group. (2) 4MC promoted the heart meter. Facial sympathetic buds, but the body surface electrocardiogram, the ventricular effective refractory period, the carotid blood pressure, the induced ventricular arrhythmia rate, and so on, there was no significant difference between the two groups in the two groups. The left myocardial tissue APD90 in the group.4MC was significantly larger than the normal group (P0.05). The two groups had no significant difference in the pricking frequency of the APD electric alternation, but the 4MC group was slightly lower than the PBS group. 1.6-OHDA makes the sympathetic denervation may reduce the occurrence of ventricular arrhythmia in rats after myocardial infarction and.2.4-MC promotes the sympathetic buds of normal rats to prolong the left ventricular monophasic action potential duration, but it does not increase the incidence of arrhythmia,.3. sympathetic nerve may participate in the onset of ventricular arrhythmia in the pathological state. Blocking the release of sympathetic neurotransmitters may reduce the occurrence of ventricular arrhythmias, even malignant ventricular arrhythmias.
【学位授予单位】：皖南医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R542.22
【参考文献】
相关期刊论文 前6条
1 姜萍;马度芳;姜月华;杨金龙;徐向东;王雪;林海青;李晓;;桂枝汤不同桂芍比例配伍对6-OHDA诱导的心脏去交感神经损伤模型大鼠心肌的保护作用[J];中国中西医结合杂志;2016年05期
2 李晓;姜萍;林海青;徐向东;杨金龙;马度芳;于潇华;姜月华;;桂枝汤对4-甲基邻苯二酚诱导心脏交感神经芽生的抑制作用[J];中国药理学通报;2014年09期
3 杨涛涛;肖颖;奚赛飞;马毅超;方明笋;寿旗扬;潘永明;陈民利;;大鼠心肌梗死模型构建和评价方法的改良[J];中国比较医学杂志;2014年02期
4 张树龙;;自主神经与心律失常[J];江苏实用心电学杂志;2012年06期
5 沙轲;陈德松;赵劲民;彭峰;陈琳;谢继辉;;大鼠颈交感神经解剖及其臂丛神经去交感神经支配模型的建立[J];中华显微外科杂志;2006年01期
6 郑先科,熊顺华,李国华;急性心肌缺血家兔心室易损期和心室颤动阈的变化[J];中国心血管杂志;2001年01期
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