Simon B C, Noll B, Maisch B
Klinik für Innere Medizin-Kardiologie, Philipps-Universität Marburg.
Herz. 1999 Feb;24(1):62-71. doi: 10.1007/BF03043820.
The vascular endothelium is the inner lining of all blood vessels and serves as an important autocrine and paracrine organ, that regulates vascular wall functions. Because of its strategic location between the circulating blood and the vascular wall, the endothelium interacts with cellular and neurohumoral mediators, thus controlling vascular contractile state and cellular composition. The vascular endothelium maintains vascular homeostasis by modulating blood vessel tone, by regulating local cellular growth and extracellular matrix deposition and by controlling hemostatic as well as inflammatory responses. One of the best characterized and most important substances released from the endothelium is nitric oxide (NO). NO is a soluble gas which is continuously synthesized from the amino acid L-arginine in endothelial cells by the constitutively expressed nitric oxide synthase. The most important stimuli represent physical factors such as shear stress and pulsatile stretching of the vessel wall as well as circulating and locally released vasoactive substances. The endothelium can be seen as a biosensor, reacting to a large variety of stimuli and therefore maintaining adequate NO release. A large number of risk factors for atherosclerosis including hypercholesterolemia, systemic hypertension, smoking and diabetes have been associated with impaired endothelial NO-mediated vasodilation. "Endothelial dysfunction" is an early marker of atherosclerosis and may be closely related to the disease process. In acute coronary syndromes dysfunctional endothelium may trigger the devastating event of plaque rupture by promoting adhesion of leukocytes, vasoconstriction, activation of platelets and thrombos formation. Atherosclerotic blood vessels are further characterized by activation through zytokines and expression of cellular adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (E-Selectin). After adhesion to the endothelium mononuclear cells migrate to the subendothelial space to take up oxidized LDL, thus transforming into foam cells, a hall mark of early atherosclerotic lesions. A number of conditions including infection with Chlamydia pneumoniae may cause continuous activation of the endothelium and inflammation of the vessel wall. Continuous endothelial dysfunction and activation, caused by risk factors and infection, represent the basis for atherogenesis and acute coronary syndromes.
血管内皮是所有血管的内层，是一个重要的自分泌和旁分泌器官，可调节血管壁功能。由于其处于循环血液与血管壁之间的关键位置，内皮与细胞和神经体液介质相互作用，从而控制血管收缩状态和细胞组成。血管内皮通过调节血管张力、调控局部细胞生长和细胞外基质沉积以及控制止血和炎症反应来维持血管稳态。内皮释放的最具特征且最重要的物质之一是一氧化氮（NO）。NO是一种可溶性气体，在内皮细胞中由持续表达的一氧化氮合酶从氨基酸L-精氨酸连续合成。最重要的刺激因素包括物理因素，如剪切应力和血管壁的搏动性拉伸，以及循环和局部释放的血管活性物质。内皮可被视为一种生物传感器，对多种刺激做出反应，从而维持适当的NO释放。包括高胆固醇血症、系统性高血压、吸烟和糖尿病在内的大量动脉粥样硬化危险因素都与内皮NO介导的血管舒张功能受损有关。“内皮功能障碍”是动脉粥样硬化的早期标志物，可能与疾病进程密切相关。在急性冠状动脉综合征中，功能失调的内皮可能通过促进白细胞黏附、血管收缩、血小板活化和血栓形成引发斑块破裂这一致命事件。动脉粥样硬化血管的进一步特征是通过细胞因子激活以及细胞黏附分子如血管细胞黏附分子-1（VCAM-1）、细胞间黏附分子-1（ICAM-1）和内皮细胞白细胞黏附分子-1（E-选择素）的表达。单核细胞黏附于内皮后迁移至内皮下间隙摄取氧化型低密度脂蛋白，从而转变为泡沫细胞，这是早期动脉粥样硬化病变的一个标志。包括肺炎衣原体感染在内的多种情况可能导致内皮持续激活和血管壁炎症。由危险因素和感染引起的持续内皮功能障碍和激活是动脉粥样硬化形成和急性冠状动脉综合征的基础。
