【摘要】：目的:心血管系統(tǒng)疾病的多發(fā)性和高發(fā)性是醫(yī)學(xué)研究的重要課題。自主神經(jīng)系統(tǒng)(包括交感神經(jīng)和副交感神經(jīng)系統(tǒng))的功能紊亂是引起各種心血管疾病的重要因素。去甲腎上腺素(NE)和乙酰膽堿(ACh)分別是傳統(tǒng)的交感神經(jīng)和副交感神經(jīng)遞質(zhì)。心臟除了受傳統(tǒng)神經(jīng)遞質(zhì)NE和ACh調(diào)節(jié)以外,還受多種神經(jīng)肽的調(diào)節(jié),它們與NE和ACh以不同組合共存于心內(nèi)神經(jīng)節(jié)細(xì)胞和神經(jīng)纖維中,并在神經(jīng)受刺激時釋放出來。各種神經(jīng)遞質(zhì)和肽類物質(zhì)不僅對心血管系統(tǒng)具有重要的生理調(diào)節(jié)作用,而且在心肌肥厚、心力衰竭等病理過程中也具有重要的作用。研究表明充血性心力衰竭發(fā)展的基本機制是心室重塑。心肌肥大是心室重塑的特征性改變。在心肌肥大的發(fā)病機理中,血流動力學(xué)作用最早為人們所重視。近年研究表明非血流動力學(xué)因素在心肌肥大發(fā)生發(fā)展過程中發(fā)揮重要作用。心肌細(xì)胞肥大是一種多因素參與調(diào)節(jié)的復(fù)雜的動態(tài)過程。能誘導(dǎo)心肌細(xì)胞發(fā)生肥大效應(yīng)的因素有許多,如神經(jīng)因素、化學(xué)因素以及機械牽拉等。其中神經(jīng)因素的調(diào)節(jié)包括交感神經(jīng)、迷走神經(jīng)、肽能神經(jīng)的調(diào)節(jié)。作為交感神經(jīng)遞質(zhì)的NE具有誘導(dǎo)心肌細(xì)胞肥大的作用已被證實。動物實驗結(jié)果顯示,長期注射亞升劑量的NE即可誘發(fā)心肌肥大,提示兒茶酚胺的促心肌細(xì)胞肥大作用除了與血流動力學(xué)效應(yīng)有關(guān)外,更為重要的是其對心肌的直接作用。作為肽能神經(jīng)遞質(zhì)的降鈣素基因相關(guān)肽(CGRP)對心肌細(xì)胞的肥大作用,國內(nèi)外文獻中曾有報道,但其觀點并不相同,有必要進一步探討CGRP對心肌細(xì)胞肥大作用的機制。作為副交感神經(jīng)遞質(zhì)的ACh對心肌細(xì)胞肥大作用的影響未見報道。因此本研究的目的是探討傳統(tǒng)神經(jīng)遞質(zhì)NE、ACh和肽類遞質(zhì)CGRP及拮抗劑作用于原代培養(yǎng)的心肌細(xì)胞,觀察單一因素對心肌細(xì)胞肥大的不同作用,進一步探討引起心肌肥大可能的機制,為臨床治療提供理論依據(jù)。 方法:將原代培養(yǎng)成活4d的大鼠心肌細(xì)胞分別加入不同濃度的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,.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R329

【引證文獻】

相關(guān)博士學(xué)位論文 前1條

1 潘孝貴;降鈣素基因相關(guān)肽對運動心臟重塑和保護作用機制的研究[D];上海體育學(xué)院;2008年

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本文編號：2387765