血管内皮功能障碍与动脉粥样硬化

内皮功能障碍是动脉粥样硬化发病的早期事件，其主要特征内皮细胞释放的内皮源性舒张因子－一氧化氮减少或其活性降低，失活增加，应用非介入性超声探测法探测肱动脉扩张反应可评估动脉血管内皮的功能状态，是检测内皮细胞的重要手段，应用降血脂，抗氧化剂，钙拮抗剂和Ｌ－精氨酸治疗动脉粥样硬化粥样硬化斑块，明显减少心血管意发生，联合治疗效果更好，故进行早期逆转内皮功能障碍的治疗对动脉粥样硬化的发病具有积极的预防作用。     

内皮功能障碍与动脉粥样硬化的关系

血管内皮可合成和释放多种内皮衍生血管活性因子,在血管自稳态调节中起重要作用.改善和提高血管内皮功能是防治动脉粥样硬化的一种新思路.     

内皮功能障碍与动脉粥样硬化的关系

血管内皮可合成和释放多种内皮衍生血管活性因子，在血管自稳态调节中起重要作用。改善和提高血管内皮功能是防治动脉粥样硬化的一种新思路。     

钙拮抗剂与血管内皮功能障碍

钙拮抗剂可选择性地抑制Ca2^＋的内流从而引起各种作用，是治疗心绞痛、高血压病、心律失常及肥厚型心肌病的理想药物。试验证明，血管内皮细胞在内分泌、抗血栓、调节血管张力等方面具有重要的生理功能，血管内皮细胞功能障碍与多种心血管疾病的病理生理过程密切相关。近年来对CAT的抗动脉粥样硬化和治疗高血压的研究表明，CAT发挥抗氧化效应进而能保护内皮细胞免受氧自由基损害，具有保护血管内皮，改善内皮功能障碍的作用。     

血管内皮功能障碍与高血压

血管内皮功能障碍与高血压密切相关。一方面血管内皮功能障碍在高血压的发生、发展过程中起重要作用;另一方面高血压本身又加重血管内皮功能障碍,形成恶性循环。现综述血管内皮细胞的生理功能、血管内皮功能障碍的相关因素、血管内皮功能障碍与高血压关系、血管内皮功能检测及血管内皮功能障碍的修复等方面的研究进展。     

血管内皮功能障碍在冠心病发生发展中的作用

在冠状动脉的动脉粥样硬化发生发展的过程中,内皮受损及内皮功能失调不仅是始动因素之一,也是其发展和转归中的重要环节。本文旨在通过对现有内皮功能与冠心病相关研究的分析来阐述内皮功能障碍在冠状动脉粥样硬化的始动、发生发展及心血管事件中的作用。     

血管内皮生长因子与动脉粥样硬化

血管内皮生长因子(VEGF)因其潜在的治疗前景引起了国内外的广泛关注。然而,近年来研究发现VEGF可促进动脉粥样硬化的发生和发展。文章就VEGF的分子特征、受体、表达调控、功能及其与动脉粥样硬化的关系作了综述。     

衰老与血管内皮功能障碍

血管内皮功能障碍是血管老化的早期病理改变之一,对动脉粥样硬化的发生发展起到非常重要的作用。老年性血管内皮功能障碍主要表现在内皮一氧化氮、前列环素和内皮衍生超极化因子等一系列内皮舒血管物质的生成减少或其生物利用度下降,而内皮素、血栓素和活性氧等一些内皮缩血管物质的生成或血管对这些物质的敏感性增加。另外,衰老导致的血管内皮修复能力减退也起到一定的作用。现就衰老对这些因素的影响及其分子机制作一概述。     

尿酸与血管内皮功能障碍的相关性

尿酸是人体核酸和嘌呤类化合物代谢的最终产物,尿酸可以通过损害血管内皮功能参与很多代谢性疾病的发生与发展．其损害内皮功能的可能机制有：尿酸产生过程中氧自由基生成增多,致一氧化氮（N0）活性降低;抑制NO合成酶的活性,减少NO的生成;直接与NO反应,降低NO的浓度;刺激炎症介质的生成,损害内皮功能。     

Primary endothelial dysfunction: atherosclerosis

The endothelium synthesizes and releases several vasodilating factors, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin. Under certain conditions, it also liberates vasocontracting factors. Thus, the endothelium plays an important role in regulating vascular homeostasis. Several intracellular mechanisms are involved in the synthesis of nitric oxide, including receptor-coupled G proteins, the availability of L-arginine, cofactors for endothelial nitric oxide synthase and the expression of the enzyme. Endothelial dysfunction by aging, menopause and hypercholesterolemia is involved in the development of atherosclerotic vascular lesions, and predisposes the blood vessel to several vascular disorders, such as vasospasm and thrombosis. Multiple mechanisms are apparently involved in the pathogenesis of the endothelial dysfunction in atherosclerosis. The reduced production of nitric oxide by the endothelium is caused by abnormalities in endothelial signal transduction, availability of L-arginine, cofactors for endothelial nitric oxide synthase and expression of the enzyme. Other mechanisms may also be involved in the impaired endothelium-dependent relaxations in atherosclerosis, including increased destruction of nitric oxide by superoxide anion, altered responsiveness of vascular smooth muscle, and concomitant release of vasocontracting factors. In addition to the treatment of the underlying risk factors, several pharmacological agents can improve endothelial dysfunction in atherosclerosis. Thus, the endothelium is a novel therapeutic target for the treatment of atherosclerotic cardiovascular disease.     

Vascular endothelial dysfunction and pharmacological treatment

The endothelium exerts multiple actions involving regulation of vascular permeability and tone, coagulation and fibrinolysis, inflammatory and immunological reactions and cell growth. Alterations of one or more such actions may cause vascular endothelial dysfunction. Different risk factors such as hypercholesterolemia, homocystinemia, hyperglycemia, hypertension, smoking, inflammation, and aging contribute to the development of endothelial dysfunction. Mechanisms underlying endothelial dysfunction are multiple, including impaired endothelium-derived vasodilators, enhanced endothelium-derived vasoconstrictors, over production of reactive oxygen species and reactive nitrogen species, activation of inflammatory and immune reactions, and imbalance of coagulation and fibrinolysis. Endothelial dysfunction occurs in many cardiovascular diseases, which involves different mechanisms, depending on specific risk factors affecting the disease. Among these mechanisms, a reduction in nitric oxide (NO) bioavailability plays a central role in the development of endothelial dysfunction because NO exerts diverse physiological actions, including vasodilation, anti-inflammation, antiplatelet, antiproliferation and antimigration. Experimental and clinical studies have demonstrated that a variety of currently used or investigational drugs, such as angiotensin-converting enzyme inhibitors, angiotensin AT1 receptors blockers, angiotensin-(1-7), antioxidants, beta-blockers, calcium channel blockers, endothelial NO synthase enhancers, phosphodiesterase 5 inhibitors, sphingosine-1-phosphate and statins, exert endothelial protective effects. Due to the difference in mechanisms of action, these drugs need to be used according to specific mechanisms underlying endothelial dysfunction of the disease.     

Vascular endothelial dysfunction in cirrhosis

Endothelial dysfunction is regarded as an early key event in multiple diseases. The assessment of vascular nitric oxide (NO) level is an indicative of endothelial dysfunction. In liver cirrhosis, on one hand, endothelial dysfunction is known as impaired endothelium-dependent relaxation in the liver microcirculation and contributes to increased intra-hepatic vascular resistance, leading to portal hypertension. On the other, increased production of vasodilator molecules mainly NO contributes to increased endothelium-dependent relaxation in the arteries of the systemic and splanchnic circulation. The aims of this review are to summarize and discuss: (1) unique characteristics of sinusoidal endothelial cell (SECs) and SEC dysfunctions in cirrhosis, and (2) endothelial dysfunctions in the arterial splanchnic and systemic circulation in cirrhosis with portal hypertension.     

吸烟、内皮细胞功能紊乱和动脉粥样硬化

吸烟是动脉粥样硬化(AS)的主要危险因素,而内皮细胞功能紊乱被认为是AS形成的关键起始因素。吸烟可通过导致内皮细胞功能紊乱,破坏内皮细胞的舒张、抗凝、抗炎等功能,增加氧化应激从而促使AS的形成。