心肌纤维化:一个慢性炎症反应过程

目的:高血压心肌纤维化发病机制复杂,炎症反应是否也参与心肌纤维化的病理生理过程?本文综述高血压发展过程中血流动力学、神经体液激素、炎症应答三者之间的联系,重点探讨炎症反应对高血压心肌纤维化的影响.资料来源:应用计算机对edline、生物医学文献数据库、中国知网数据库检索1991-01/2007-05期间与炎症反应对高血压心肌纤维化影响相关文献,包括临床和基础研究.中文检索词包括“高血压“,“心肌纤维化“,“炎症反应“,“血管紧张素“和“细胞因子“;英文检索词有“hypertension“,“myocardial fibrosis“,“inflammatory response“,“angiotensin“ “cytokines“.资料选择:对检索到的文献进行初审,选择文献所述内容与高血压心肌纤维化时炎症反应作用相关的文献.排除重复性研究和Meta分析类文章.资料提炼:共收集到相关文献641篇,阅读全部文章的文题和大部分文章的摘要.符合纳入条件的文献162篇,选择其中42篇文献进行分析.资料综合:高血压过程中,心肌间质因为反应性纤维化和修复性纤维化而扩展,最终导致心肌纤维化的发生.临床和实验研究表明血流动力学和神经体液激素影响了心肌纤维化的过程.目前越来越多的研究提示,在高血压心肌纤维化的过程中,在血流动力学和神经体液激素的影响下免疫系统也被激活.随后招募的各种炎症细胞和因子,包括趋化蛋白、黏附分子和细胞因子,形成细胞因子串联反应,加剧心肌纤维化的发展速度.结论:炎症反应参与了高血压心肌纤维化的病理生理过程,加快心力衰竭的发生发展.

Myocardial fibrosis: A chronic inflammatory process

OBJECTIVE:The pathophysiology of myocardial fibrosis during hypertension is complicated.Recently,it has been shown that inflammatory response plays an important role in the pathophysiology of myocardial fibrosis.This review describes the relationships among hemodynamic stress,hormonal factors and inflammatory factors,and emphasizes the important position of inflammation during the progress of myocardial fibrosis.DATA SOURCES:Using the terms of "hypertension,myocardial fibrosis,inflammatory response,angiotensin,cytokines" in English and Chinese respectively,we searched Medline database,Chinese Biological Medicine Database (CBM) and CNKI to identify English and Chinese articles of clinical researches and experiments related to the effects of inflammatory response on myocardial fibrosis during hypertension published from January 1991 to May 2007.STUDY SELECTION:The articles were primarily checked.Only articles that reported inflammatory response and myocardial fibrosis were included.The repeated researches and experiments and Meta analysis were deleted.DATA EXTRACTION:A total of 641 articles have been selected.The titles of all the articles and most of the abstracts have been read,and 162 articles met the inclusive criteria whereas the other 479 articles were deleted.42 articles have been analyzed.DATA SYNTHESIS:During hypertension,the extracellular matrix expands because of reactive and reparative fibrosis,which at last results in myocardial fibrosis.Previous clinical and experimental studies showed that hemodynamic stress and hormonal factors affected the progress of myocardial fibrosis.While recently,there are growing evidences indicating that the immune system.related with hemodynamic stress and hormonal factors is activated during hypertension in the progress of myocardial fibrosis.Then the recruitment of inflammatory cells and factors,including chemoattractant proteins,adhesion molecules and cytokines,informing cytokines cascade response,in turn accelerate the progress of myocardial fibrosis.CONCLUSION:Inflammatory response may play an important role in the pathophysiology of myocardial fibrosis during hypertension and then accelerate the progress of heart failure.