交感神經(jīng)放電對大鼠心室電生理影響的研究
發(fā)布時(shí)間：2018-08-08 17:57
【摘要】：目的:學(xué)習(xí)大鼠心肌梗死模型的制作,建立測量頸交感神經(jīng)電活動(dòng)的方法及單電極測定心室肌表面單相動(dòng)作電位,以探索交感神經(jīng)在大鼠心肌梗死后室性心律失常的作用及促進(jìn)正常大鼠心臟表面交感神經(jīng)芽生是否使大鼠更易發(fā)生心律失常。方法:麻醉狀態(tài)下,氣管插管,開胸并在左心耳下緣結(jié)扎大鼠冠狀動(dòng)脈前降支,使前壁心肌細(xì)胞急性缺血以制作心肌梗死模型。切開頸前皮膚,找到頸交感神經(jīng),剝離交感神經(jīng)束外膜,并與外周肌肉及軟組織隔離,連接電生理儀測定頸交感神經(jīng)電活動(dòng)。(1)6-羥多巴胺(6-hydroxydopamine,6-OHDA)去交感神經(jīng)支配模型:大鼠隨機(jī)分為假手術(shù)組(sham+Vc)、假手術(shù)對照組(sham+6-OHDA)、心肌梗死組(AMI+Vc)和心肌梗死對照組(AMI+6OHDA),sham+6-OHDA組和AMI+6OHDA組用6-羥多巴胺(6OHDA)化學(xué)性去除交感神經(jīng)3天,sham+Vc和AMI+Vc予以等劑量的0.2%維生素C溶劑。在麻醉并氣管插管下,監(jiān)測體表心電圖、頸交感神經(jīng)電活動(dòng)、頸動(dòng)脈血壓,程序刺激(Programmed Electrical Stimulation,PES)測量心室有效不應(yīng)期(Ventricular Effective Refractory Period,VERP)、室性心律失常。(2)4-甲基鄰苯二酚(4-methylcatechol,4-MC)促進(jìn)心臟表面交感神經(jīng)芽生模型。大鼠被隨機(jī)分為正常組(Phosphate Buffer Solution,PBS)和實(shí)驗(yàn)組(4-MC),實(shí)驗(yàn)組予以4-MC腹腔注射30天以促進(jìn)交感神經(jīng)芽生,正常組予以等劑量PBS溶劑。麻醉后測量體表心電圖、頸交感神經(jīng)電活動(dòng)、頸動(dòng)脈血壓、及心室表面電生理。結(jié)果:(1)AMI+Vc組RR值明顯大于其他三組(P0.05),AMI+Vc組QRS波明顯大于sham+Vc組和AMI+6OHDA組,AMI+Vc組QT間期明顯大于sham+Vc組和AMI+6OHDA組(P0.05),而P波、PR間期、ERP在各組間無統(tǒng)計(jì)學(xué)差異。AMI+Vc組非梗死區(qū)APD50、APD90較sham+VC組及sham+6-OHDA組顯著延長(P0.05),AMI+Vc組梗死周邊區(qū)APD50、APD90較其他三組顯著延長(P0.05)。各組間的APD電交替頻率沒有統(tǒng)計(jì)學(xué)差別,但心肌梗死后的頻率低于非梗死組。AMI+Vc組大鼠更易誘發(fā)出室性心律失常,給予6-OHDA的大鼠均未誘導(dǎo)出心律失常。大鼠頸交感神經(jīng)放電活動(dòng)增加后可誘發(fā)室性心律失常,給予6-OHDA后未見室性心律失常的發(fā)生。心肌梗死及6-OHDA阻斷交感神經(jīng)后,頸動(dòng)脈壓沒有明顯統(tǒng)計(jì)學(xué)差別,但較sham+Vc組血壓下降。(2)4MC促進(jìn)心臟表面交感神經(jīng)芽生,但體表心電圖、心室有效不應(yīng)期、頸動(dòng)脈血壓、誘發(fā)室性心律失常率等在兩組間沒有明顯的統(tǒng)計(jì)學(xué)差異。4MC組左心肌組織APD90明顯大于正常組(P0.05)。兩組比較引起APD電交替的刺激頻率無明顯差別,但4MC組稍低于PBS組。結(jié)論:1.6-OHDA使交感神經(jīng)去支配可能減少了心肌梗死后大鼠室性心律失常的發(fā)生。2.4-MC促進(jìn)正常大鼠的交感神經(jīng)芽生可使其左側(cè)心室單相動(dòng)作電位時(shí)程延長,但并不增加心律失常發(fā)生率。3.交感神經(jīng)可能參與了病理狀態(tài)下室性心律失常的發(fā)生,且阻斷交感神經(jīng)神經(jīng)遞質(zhì)的釋放可能會(huì)減少室性心律失常、甚至是惡性室性心律失常的發(fā)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.
【學(xué)位授予單位】：皖南醫(yī)學(xué)院
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R542.22
本文編號：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.
【學(xué)位授予單位】：皖南醫(yī)學(xué)院
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R542.22
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