Endothelial dysfunction in human disease
Endothelial dysfunction in human disease
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DOI：
10.1006/jmcc.1998.0843
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发表时间：
1999-01-01
影响因子：
5
通讯作者：
Hornig, B
中科院分区：
文献类型：
--
作者：
Drexler, H;Hornig, B
血管内皮通过释放血管舒张剂物质（即内皮来源的松弛因子（EDRF =一氧化氮））在局部调节血管张力中起关键作用。NO)和前列环素)和血管收缩物质（即血栓素A、自由基或内皮素）。临床研究表明，使用乙酰胆碱等药物或改变血流来刺激EDRF （NO）的释放，EDRF在心外膜大冠状动脉和冠状微循环血管张力的基础和刺激控制中都具有重要作用。内皮的调节功能可被心血管危险因素或疾病如高胆固醇血症、慢性熔炼、高血压或慢性心力衰竭所改变。内皮功能障碍似乎具有有害的功能后果以及不利的长期影响，包括血管重构。内皮功能障碍与组织灌注受损有关，特别是在应激和包括冠状动脉在内的大导管血管的矛盾收缩时。这些作用可能导致或促成心肌缺血。内皮功能障碍的发生可能涉及多种机制，如EDRF的合成和释放减少，或EDRF被自由基或氧化低密度脂蛋白（LDL）从内皮细胞释放后，EDRF的失活加剧。慢性吸烟者血浆中氧化LDL水平升高与内皮功能障碍的程度有关，这增加了慢性吸烟通过增加循环和组织中氧化LDL水平而加剧内皮功能障碍的可能性。在心力衰竭中，细胞因子和/或血流减少（反映剪切应力减少）可能参与内皮功能障碍的发展，并可通过体育训练逆转。其他机制包括激活肾素-血管紧张素系统（即心肌梗死后），通过增强血管紧张素转换酶（ACE）活性增加缓激素的分解。有证据表明，内源性缓激肽参与冠状动脉导管和阻力血管的血管舒缩控制。ACE抑制剂通过缓激肽依赖机制增强内皮功能，也可能通过抑制超氧阴离子的产生。内皮功能障碍似乎可以通过给予l -精氨酸而逆转。一氧化氮的前体。降低胆固醇水平，体育锻炼，抗氧化剂，如维生素C，或抑制ACE。(C) 1999学术出版社。
The vascular endothelium plays a key role in the local regulation of vascular tone by the release of vasodilator substances (i.e. endothelium-derived relaxing factor (EDRF = nitric oxide. NO) and prostacyclin) and vasoconstrictor substances (i.e. thromboxane A,, free radicals, or endothelin). Using either agents like acetylcholine or changes in flow to stimulate the release of EDRF (NO), clinical studies have revealed the importance of EDRF in both basal and stimulated control of vascular tone in large epicardial coronary arteries and in the coronary microcirculation. The regulatory function of the endothelium is altered by cardiovascular risk factors or disorders such as hypercholesterolemia, chronic smelting, hypertension or chronic heart failure. Endothelial dysfunction appears to have detrimental functional consequences as well as adverse longterm effects, including vascular remodelling. Endothelial dysfunction is associated with impaired tissue perfusion particularly during stress and paradoxical vasoconstriction of large conduit vessels including the coronary arteries. These effects may cause or contribute to myocardial ischemia. Several mechanisms may be involved in the development of endothelial dysfunction, such as reduced synthesis and release of EDRF or enhanced inactivation of EDRF after its release from endothelial cells by radicals or oxidized low-density lipoprotein (LDL). Increased plasma levels of oxidized LDL have been noted in chronic smokers and are related to the extent endothelial dysfunction, raising the possibility that chronic smoking potentiates endothelial dysfunction by increasing circulating and tissue levels of oxidized LDL. In heart failure, cytokines and/or reduced flow (reflecting reduced shear stress) may be involved in the development of endothelial dysfunction and can be reversed by physical training. Other mechanisms include an activated renin-angiotensin system (i.e. postmyocardial infarction) with increased breakdown of bradykinin by enhanced angiotensin converting enzyme (ACE) activity. There is evidence that endogenous bradykinin is involved in coronary vasomotor control both in coronary conduit and resistance vessels. ACE inhibitors enhance endothelial function by a bradykinin-dependent mechanism and probably also by blunting the generation of superoxide anion. Endothelial dysfunction appears to be reversible by administering L-arginine. the precursor of nitric oxide. lowering cholesterol levels, physical training, antioxidants such as vitamin C, or ACE inhibition. (C) 1999 Academic Press.