CGRP与NE和ACh对心肌细胞影响作用的研究
发布时间：2018-12-20 09:06
【摘要】：目的:心血管系统疾病的多发性和高发性是医学研究的重要课题。自主神经系统(包括交感神经和副交感神经系统)的功能紊乱是引起各种心血管疾病的重要因素。去甲肾上腺素(NE)和乙酰胆碱(ACh)分别是传统的交感神经和副交感神经递质。心脏除了受传统神经递质NE和ACh调节以外,还受多种神经肽的调节,它们与NE和ACh以不同组合共存于心内神经节细胞和神经纤维中,并在神经受刺激时释放出来。各种神经递质和肽类物质不仅对心血管系统具有重要的生理调节作用,而且在心肌肥厚、心力衰竭等病理过程中也具有重要的作用。研究表明充血性心力衰竭发展的基本机制是心室重塑。心肌肥大是心室重塑的特征性改变。在心肌肥大的发病机理中,血流动力学作用最早为人们所重视。近年研究表明非血流动力学因素在心肌肥大发生发展过程中发挥重要作用。心肌细胞肥大是一种多因素参与调节的复杂的动态过程。能诱导心肌细胞发生肥大效应的因素有许多,如神经因素、化学因素以及机械牵拉等。其中神经因素的调节包括交感神经、迷走神经、肽能神经的调节。作为交感神经递质的NE具有诱导心肌细胞肥大的作用已被证实。动物实验结果显示,长期注射亚升剂量的NE即可诱发心肌肥大,提示儿茶酚胺的促心肌细胞肥大作用除了与血流动力学效应有关外,更为重要的是其对心肌的直接作用。作为肽能神经递质的降钙素基因相关肽(CGRP)对心肌细胞的肥大作用,国内外文献中曾有报道,但其观点并不相同,有必要进一步探讨CGRP对心肌细胞肥大作用的机制。作为副交感神经递质的ACh对心肌细胞肥大作用的影响未见报道。因此本研究的目的是探讨传统神经递质NE、ACh和肽类递质CGRP及拮抗剂作用于原代培养的心肌细胞,观察单一因素对心肌细胞肥大的不同作用,进一步探讨引起心肌肥大可能的机制,为临床治疗提供理论依据。 方法:将原代培养成活4d的大鼠心肌细胞分别加入不同浓度的NE、
[Abstract]:Objective: the multiple and high incidence of cardiovascular diseases is an important subject in medical research. The dysfunction of autonomic nervous system (including sympathetic and parasympathetic nervous systems) is an important cause of various cardiovascular diseases. Norepinephrine (NE) and acetylcholine (ACh) are traditional sympathetic neurotransmitters and parasympathetic neurotransmitters, respectively. The heart is regulated not only by the traditional neurotransmitters NE and ACh, but also by a variety of neuropeptides, which coexist in different combinations with NE and ACh in the intracardiac ganglion cells and nerve fibers, and are released when the nerve is stimulated. Neurotransmitters and peptides not only play an important role in regulating cardiovascular system, but also play an important role in myocardial hypertrophy, heart failure and other pathological processes. Studies have shown that ventricular remodeling is the basic mechanism for the development of congestive heart failure. Myocardial hypertrophy is the characteristic change of ventricular remodeling. Among the pathogenesis of myocardial hypertrophy, hemodynamics was paid more attention. Recent studies have shown that non-hemodynamic factors play an important role in the development of myocardial hypertrophy. Cardiomyocyte hypertrophy is a complex dynamic process in which many factors are involved in regulation. There are many factors that can induce hypertrophy of cardiomyocytes, such as nerve factors, chemical factors and mechanical pull. The regulation of neural factors includes the regulation of sympathetic nerve, vagus nerve and peptidergic nerve. It has been proved that NE, as a sympathetic neurotransmitter, can induce cardiac myocyte hypertrophy. The results of animal experiments showed that long-term injection of NE could induce myocardial hypertrophy, suggesting that catecholamine induced cardiac hypertrophy not only related to hemodynamic effects, but also more important to the direct action of catecholamine on myocardium. The effect of calcitonin gene-related peptide (CGRP) on cardiomyocyte hypertrophy has been reported in the literature at home and abroad, but its views are different. It is necessary to further explore the mechanism of CGRP on cardiomyocyte hypertrophy. The effect of parasympathetic neurotransmitter ACh on cardiomyocyte hypertrophy has not been reported. The aim of this study was to investigate the effects of traditional neurotransmitter NE,ACh, peptide transmitter CGRP and antagonist on primary cultured cardiomyocytes, and to observe the different effects of single factor on cardiomyocyte hypertrophy. To explore the possible mechanism of myocardial hypertrophy and provide theoretical basis for clinical treatment. Methods: primary cultured rat cardiomyocytes were cultured for 4 days with different concentrations of NE,.
【学位授予单位】：山东大学
【学位级别】：硕士
【学位授予年份】：2005
【分类号】：R329
本文编号：2387765
[Abstract]:Objective: the multiple and high incidence of cardiovascular diseases is an important subject in medical research. The dysfunction of autonomic nervous system (including sympathetic and parasympathetic nervous systems) is an important cause of various cardiovascular diseases. Norepinephrine (NE) and acetylcholine (ACh) are traditional sympathetic neurotransmitters and parasympathetic neurotransmitters, respectively. The heart is regulated not only by the traditional neurotransmitters NE and ACh, but also by a variety of neuropeptides, which coexist in different combinations with NE and ACh in the intracardiac ganglion cells and nerve fibers, and are released when the nerve is stimulated. Neurotransmitters and peptides not only play an important role in regulating cardiovascular system, but also play an important role in myocardial hypertrophy, heart failure and other pathological processes. Studies have shown that ventricular remodeling is the basic mechanism for the development of congestive heart failure. Myocardial hypertrophy is the characteristic change of ventricular remodeling. Among the pathogenesis of myocardial hypertrophy, hemodynamics was paid more attention. Recent studies have shown that non-hemodynamic factors play an important role in the development of myocardial hypertrophy. Cardiomyocyte hypertrophy is a complex dynamic process in which many factors are involved in regulation. There are many factors that can induce hypertrophy of cardiomyocytes, such as nerve factors, chemical factors and mechanical pull. The regulation of neural factors includes the regulation of sympathetic nerve, vagus nerve and peptidergic nerve. It has been proved that NE, as a sympathetic neurotransmitter, can induce cardiac myocyte hypertrophy. The results of animal experiments showed that long-term injection of NE could induce myocardial hypertrophy, suggesting that catecholamine induced cardiac hypertrophy not only related to hemodynamic effects, but also more important to the direct action of catecholamine on myocardium. The effect of calcitonin gene-related peptide (CGRP) on cardiomyocyte hypertrophy has been reported in the literature at home and abroad, but its views are different. It is necessary to further explore the mechanism of CGRP on cardiomyocyte hypertrophy. The effect of parasympathetic neurotransmitter ACh on cardiomyocyte hypertrophy has not been reported. The aim of this study was to investigate the effects of traditional neurotransmitter NE,ACh, peptide transmitter CGRP and antagonist on primary cultured cardiomyocytes, and to observe the different effects of single factor on cardiomyocyte hypertrophy. To explore the possible mechanism of myocardial hypertrophy and provide theoretical basis for clinical treatment. Methods: primary cultured rat cardiomyocytes were cultured for 4 days with different concentrations of NE,.
【学位授予单位】：山东大学
【学位级别】：硕士
【学位授予年份】：2005
【分类号】：R329
【引证文献】
相关博士学位论文 前1条
1 潘孝贵;降钙素基因相关肽对运动心脏重塑和保护作用机制的研究[D];上海体育学院;2008年
，本文编号：2387765
本文链接：https://www.wllwen.com/yixuelunwen/binglixuelunwen/2387765.html
最近更新
教材专著
