中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
7期
1319-1324
,共6页
高血压%心室重构%炎症介质
高血壓%心室重構%炎癥介質
고혈압%심실중구%염증개질
Hypertension%Ventricular remodeling%Inflammatory mediators
左心室重构作为高血压靶器官损害之一,与心脏事件、心脏外靶器官损害均密切相关。高血压左心室重构受到机械刺激、神经体液因素和炎症反应等多种因素影响。多种炎症介质可通过影响心肌细胞生长、心脏成纤维细胞转化和分泌基质蛋白,改变细胞外基质的含量与组成以及改变冠状动脉的结构与功能而影响高血压左心室重构的发生和发展。此外,炎症介质还可相互作用,并参与介导高血压左心室重构的机械负荷和神经体液机制,组成复杂的网络系统,从多个靶点、多个环节对高血压左心室重构产生重要影响。临床常用降压药ACEI和CCB均可通过作用于炎症介质而延缓和(或)逆转高血压左心室重构的进程。
左心室重構作為高血壓靶器官損害之一,與心髒事件、心髒外靶器官損害均密切相關。高血壓左心室重構受到機械刺激、神經體液因素和炎癥反應等多種因素影響。多種炎癥介質可通過影響心肌細胞生長、心髒成纖維細胞轉化和分泌基質蛋白,改變細胞外基質的含量與組成以及改變冠狀動脈的結構與功能而影響高血壓左心室重構的髮生和髮展。此外,炎癥介質還可相互作用,併參與介導高血壓左心室重構的機械負荷和神經體液機製,組成複雜的網絡繫統,從多箇靶點、多箇環節對高血壓左心室重構產生重要影響。臨床常用降壓藥ACEI和CCB均可通過作用于炎癥介質而延緩和(或)逆轉高血壓左心室重構的進程。
좌심실중구작위고혈압파기관손해지일,여심장사건、심장외파기관손해균밀절상관。고혈압좌심실중구수도궤계자격、신경체액인소화염증반응등다충인소영향。다충염증개질가통과영향심기세포생장、심장성섬유세포전화화분비기질단백,개변세포외기질적함량여조성이급개변관상동맥적결구여공능이영향고혈압좌심실중구적발생화발전。차외,염증개질환가상호작용,병삼여개도고혈압좌심실중구적궤계부하화신경체액궤제,조성복잡적망락계통,종다개파점、다개배절대고혈압좌심실중구산생중요영향。림상상용강압약ACEI화CCB균가통과작용우염증개질이연완화(혹)역전고혈압좌심실중구적진정。
As one of the hypertensive target organ damage, left ventricular remodeling is closely related to heart attacks and extracardiac target organ damage. Left ventricular remodeling of hypertension is influenced by mechanical stimuli, neurohumoral factors, inflammation, ect. Many kinds of inflammatory mediators affect the onset and process of hypertensive left ventricular remodeling by influencing myocardial cell growth, cardiac fibroblasts transforming and secreting matrix proteins, changing the content and composition of extracellular matrix, and changing the structure and function of coronary arteries. In addition, inflammatory mediators interact with each other, and participate in the mechanical and neurohumoral mechanisms of hypertensive left ventricular remodeling, thus composing a complex network system, which influences left ventricular remodeling of hypertension greatly by multiple targets and pathways. Common clinical antihypertensive drugs such as ACEI and CCB can delay and/or reverse left ventricular remodeling of hypertension process by acting on inflammatory mediators.