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恰加斯病与自主神经系统受累

Chagas' disease and the involvement of the autonomic nervous system.

作者信息

da Cunha Ademir Batista

机构信息

Universidade Federal Fluminense, Instituto Nacional de Cardiología, Rio de Janeiro, Brasil.

出版信息

Rev Port Cardiol. 2003 Jun;22(6):813-24.

Abstract

Chagas' disease is a major endemic disease in Latin America and a great cause for concern due to its high incidence: it afflicts 16 to 18 million individuals and places over 90 million people at risk of infection. At present, five mechanisms can be proposed to explain the pathogenesis of chronic Chagas cardiopathy: 1. direct lesion of the tissue by Trypanosoma cruzi; 2. dysfunction of the autonomic nervous system (neurogenic concept); 3. microvascular disease; 4. immunologic reaction; 5. alterations in the extracellular matrix. The neurogenic concept is the most attractive explanation for the pathogenesis of chronic Chagas cardiopathy through the involvement of the autonomic nervous system, an issue that has been prominent ever since Chagas first initiated research in the field. Köberle, in his pioneering studies on the role of the autonomic nervous system in Chagas patients in the 1950s, adopted the technique of neuron counts, whereby he registered a reduction in parasympathetic nerve cells, and thus considered Chagas cardiopathy a "parasympathetic reduction" with predominance of the sympathetic. In the 1960s, systematic studies on autonomic function, organized by Professor Dalmo Amorim, were initiated in the School of Medicine in Ribeirão Preto. Several aspects of cardiac autonomic control were later described independently by teams in Brazil (Ribeirão Preto and Brasília), Argentina (Cordoba) and Venezuela (Mérida). In general, the studies performed in Ribeirăo Preto by Amorim and Marin Neto and in Brasília by Junqueira Jr. reflected the functional involvement of the parasympathetic system, while the studies performed in Córdoba were linked with the view of cardiovascular sympathetic dysfunction. In Brazil, the involvement of the sympathetic system, with relation to the functional aspect of sympathetic denervation, is well characterized by Marin Neto through the assessment of heart rate using the tilt test in both Chagas and control groups. Further evidence of autonomic nervous system dysfunction in Chagas' disease as a factor modulating complex ventricular arrhythmias was demonstrated by Pedrosa (RJ), who reported on a specific group of chronic Chagas patients with complex ventricular arrhythmias and dilated cardiopathy. In this study, when serum from chronic Chagas patients showing neither complex ventricular arrhythmias nor ventricular dilation was inoculated in isolated rabbit hearts, it produced no harmful effect in the conduction system, in contrast to what was observed in the conduction system of rabbits inoculated with serum from the Chagas patients group with complex ventricular arrhythmias and ventricular dilatation. These facts confirm Carlos Chagas as the pioneer in postulating involvement of the autonomic nervous system in Chagas' disease, and provide an important opportunity to understand ventricular involvement in chronic Chagas cardiopathy.

摘要

恰加斯病是拉丁美洲的一种主要地方病,因其高发病率而备受关注:该病折磨着1600万至1800万人,并使9000多万人面临感染风险。目前,可以提出五种机制来解释慢性恰加斯心肌病的发病机制:1. 克氏锥虫对组织的直接损害;2. 自主神经系统功能障碍(神经源性概念);3. 微血管疾病;4. 免疫反应;5. 细胞外基质改变。神经源性概念是通过自主神经系统的参与来解释慢性恰加斯心肌病发病机制最具吸引力的解释,自恰加斯首次开展该领域研究以来,这个问题就一直很突出。20世纪50年代,科贝雷在其关于自主神经系统在恰加斯病患者中作用的开创性研究中,采用了神经元计数技术,据此他记录到副交感神经细胞减少,因此认为恰加斯心肌病是一种以交感神经占主导的“副交感神经减少”。20世纪60年代,由达尔莫·阿莫林教授组织的关于自主神经功能的系统研究在里贝朗普雷图医学院启动。后来,巴西(里贝朗普雷图和巴西利亚)、阿根廷(科尔多瓦)和委内瑞拉(梅里达)的研究团队分别独立描述了心脏自主控制的几个方面。一般来说,阿莫林和马林·内托在里贝朗普雷图进行的研究以及小容凯拉在巴西利亚进行的研究反映了副交感神经系统的功能参与,而在科尔多瓦进行的研究则与心血管交感神经功能障碍的观点相关。在巴西,马林·内托通过对恰加斯病患者和对照组使用倾斜试验评估心率,很好地描述了交感神经系统在交感神经去神经功能方面的参与情况。佩德罗萨(里约热内卢)证明了恰加斯病中自主神经系统功能障碍作为调节复杂室性心律失常的一个因素的进一步证据,他报告了一组患有复杂室性心律失常和扩张型心肌病的慢性恰加斯病患者。在这项研究中,将既无复杂室性心律失常也无心室扩张的慢性恰加斯病患者的血清接种到离体兔心脏中时,对传导系统没有产生有害影响,这与接种患有复杂室性心律失常和心室扩张的恰加斯病患者组血清的兔子传导系统中观察到情况相反。这些事实证实卡洛斯·恰加斯是假设自主神经系统参与恰加斯病的先驱,并为理解慢性恰加斯心肌病中心室受累情况提供了重要契机。

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