Cardiac autonomic nerve distribution and arrhythmia

OBJECTIVE： To analyze the distribution characteristics of cardiac autonomic nerves and to explore the correlation between cardiac autonomic nerve distribution and arrhythmia. DATA RETRIEVAL： A computer-based retrieval was performed for papers examining the distribution of cardiac autonomic nerves, using “heart, autonomic nerve, sympathetic nerve, vagus nerve, nerve distribution, rhythm and atrial fibrillation” as the key words. SELECTION CRITERIA： A total of 165 studies examining the distribution of cardiac autonomic nerve were screened, and 46 of them were eventually included. MAIN OUTCOME MEASURES： The distribution and characteristics of cardiac autonomic nerves were observed, and immunohistochemical staining was applied to determine the levels of tyrosine hydroxylase and acetylcholine transferase （main markers of cardiac autonomic nerve distribution）. In addition, the correlation between cardiac autonomic nerve distribution and cardiac arrhythmia was investigated. RESULTS： Cardiac autonomic nerves were reported to exhibit a disordered distribution in different sites, mainly at the surface of the cardiac atrium and pulmonary vein, forming a ganglia plexus. The distribution of the pulmonary vein autonomic nerve was prominent at the proximal end rather than the distal end, at the upper left rather than the lower right, at the epicardial membrane rather than the endocardial membrane, at the left atrium rather than the right atrium, and at the posterior wall rather than the anterior wall. The main markers used for cardiac autonomic nerves were tyrosine hydroxylase and acetylcholine transferase. Protein gene product 9.5 was used to label the immunoreactive nerve distribution, and the distribution density of autonomic nerves was determined using a computer-aided morphometric analysis system. CONCLUSION： The uneven distribution of the cardiac autonomic nerves is the leading cause of the occurrence of arrhythmia, and the cardiac autonomic nerves play an important role in the occurrence, maintenance, and symptoms of arrhythmia.

槲寄生提取物抗缺血性心律失常作用的研究

目的研究槲寄生提取物(viscum coloratum extract,VCE)抗缺血性心律失常的药理作用。方法采用大鼠冠脉结扎的方法建立心肌梗死模型,观察VCE对心肌梗死大鼠心律失常发生率和心肌梗死面积的影响。制备大鼠离体右心房标本,在浴槽中观察VCE对大鼠右心房收缩性的影响。结果注射VCE各组与对照组比,心律失常发生减少,心肌梗死面积缩小。低剂量VCE可使大鼠离体右心房收缩力呈现正性肌力,而高剂量VCE呈现负性肌力。VCE的负性肌力作用可被阿托品阻断。高剂量VCE可使大鼠离体右心房收缩频率降低;VCE能使异丙肾上腺素对心肌的收缩作用降低;使CaCl2量效曲线下移。结论 VCE有抗缺血性心律失常的作用,高剂量VCE能使大鼠离体右心房表现为负性肌力和负性频率作用,还能对抗异丙肾上腺素和CaCl2的正性作用,VCE的负性肌力作用可被阿托品阻断提示其抗缺血性心律失常作用可能与激动M受体或其某一亚型有关。

毛果芸香碱对实验性心律失常的保护作用

目的:观察毛果芸香碱对实验性心率失常的影响。方法:分别以乌头碱,氯化钡和哇巴因制备实验性动物心律失常模型。观察毛果芸香碱的干预作用。结果:毛果芸香碱可显著延迟乌头碱引起的大鼠室性心律失常的出现(P<0.05),延长出现心律失常后的存活时间(P<0.05);能明显延迟氯化钡引起的大鼠双相室性心律失常的出现(P<0.01).缩短心律失常的持续时间(P<0.01);能显著延长哇巴因引起豚鼠出现心律失常后的存活时间(P<0.05)。毛果芸香碱的上述作用可被M_3受体阻断剂4-DAMP完全逆转。结论:毛果芸香碱具有对抗乌头碱和氯化钡诱发大鼠,哇巴因诱发豚鼠心律失常的作用,提示其具有良好的抗心律失常作用;毛果芸香碱通过激动大鼠和豚鼠心肌M_3受体而产生抗心律失常的作用。

毛果芸香碱对心律失常保护作用的研究

目的观察毛果芸香碱对动物心律失常模型的作用。方法分别以乌头碱和氯化钡制造动物心律失常模型,观察毛果芸香碱(0.2mg/kg)对心律失常的影响。结果毛果芸香碱可明显延迟乌头碱引起的大鼠室性心律失常的出现(P<0.05);延长大鼠出现心律失常后的存活时间(P<0.05);毛果芸香碱可明显延迟氯化钡引起的大鼠双向室性心律失常的出现(P<0.05)、缩短大鼠心律失常的持续时间(P<0.05)。4-DAMP可完全拮抗毛果芸香碱诱导的心律失常。结论毛果芸香碱通过激动大鼠心肌M3受体而产生对抗乌头碱和氯化钡诱发大鼠心律失常的作用。

匹鲁卡品对Wistar大鼠心律失常的影响

目的观察匹罗卡品对Wistar大鼠心律失常的作用。方法分别以乌头碱、氯化钡制作Wistar大鼠心律失常模型,观察0.2 mg.kg-1匹罗卡品舌下静脉注射对心律失常的作用。结果匹罗卡品可明显延迟乌头碱引起Wistar大鼠室性心律失常的出现(P<0.05)、延长其出现心律失常后的存活时间(P<0.05);匹罗卡品能明显延迟氯化钡引起Wistar大鼠双相室性心律失常的出现(P<0.01)、缩短其心律失常的持续时间(P<0.01);但上述作用可被M3受体阻滞剂4-DAMP完全逆转。结论匹罗卡品通过激动Wistar大鼠心肌M3受体而产生对抗乌头碱和氯化钡诱发Wistar大鼠心律失常的作用。