容量负荷与心室结构重建的研究进展  

Advances in volume overload-induced ventricular structural remodeling

作　　者：张超英[1] 李晓惠[1] 

机构地区：[1]首都儿科研究所附属儿童医院内科,北京100020

出　　处：《中国病理生理杂志》2011年第2期403-406,416,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30872787);北京市优秀人才培养资助项目(No.20081D0303200107);北京市卫生局青年科学研究资助项目(No.QN2007-08)

摘　　要：容量负荷即心脏的前负荷,是指心肌收缩之前遇到的负荷。在生理范围,适度前负荷增加,则心肌收缩力增强,每搏量增加;但若前负荷过度增加,则使心肌收缩力减弱,每搏量减少;前负荷增加持续存在,则心室腔代偿性扩张,即离心性心脏肥大,最终导致心力衰竭。有关心力衰竭的研究已有300余年的历史。Many cardiovascular diseases were characterized by cardiac volume overload. Chronic volume overload induces ventricular structural remodeling, and then results in cardiac dysfunction and heart failure in the end. It has been reported that the activation of sympathetic nervous system（SNS） is one of the fastest and earliest compensatory mechanism in the process of volume overload. However, chronic activation of SNS causes the elevation of catecholamine concentration, resulting in cardio - toxicity. Rennin - angiogenesis - aldosterone system（RAAS） in cardiac region rather than systemic blood circulation plays a main role in ventricular structural remodeling. Inflammatory cytokines, such as tumor necro- sis factor α9, interleukin 113 and interleukin 6, participate in volume overload - induced ventricular structural remodeling. Increased expression of matrix metalloproteinase 2,3,9 and decreased expression of tissue inhibitors of matrix metaUoprotease 1 are also involved in the pathogenesis of ventricular structural remodeling. The elevated protein expression of collagen I and collagen Ⅲ in volume overload leads to cardiac hypertrophy. Endothelial nitric oxide synthase and neural nitric ox- ide synthase regulate the production of nitric oxide by positive feedback, but inducible nitric oxide synthase by negative feedback of ventricular structural remodeling. Peroxisome proliferator activated receptor γand their ligands reverse ventricular structural remodeling by resisting neuroendocrine function.

关 键 词：容量负荷 心室重建 

分 类 号：R541.6[医药卫生—心血管疾病]