从内皮生理机制看支架术后再内皮化的重要性.pptVIP

* 大量的研究发现：第一代DES(SES/PES)较BMS加强了血管收缩，在很多临床病例报告中都记载了SES和PES之后冠脉血管严重、广泛的血管痉挛发生。这种现象可能的原因是血流减少以及支架血管内不正常的血流，这些都能增加炎症和血栓的风险，其中DES引发的内皮愈合不良和内皮功能紊乱是引发血管痉挛、晚期血栓的基本机制。 In general, the 1st-gen DES have shown to enhance vasoconstriction when compared with BMS. This lower set point for contraction might be anticipated to cause adverse effects on distal myocardial perfusion and regional myocardial function. Indeed, severe diffuse coronary artery spasm after both PES and SES was well-documented in clinical case reports (50–54). So far, the potential contribution of such ?ow pattern impairment to DES thrombosis is still unknown.We postulate that this phenomenon would result in blood ?ow reduction and exacerbation of nonlaminar ?ow within the stented vessel, which likely link to increases in in?ammatory and thrombotic risks (Fig. 2). Although many factors such as patient, lesion, as well as procedural characteristics are likely contributory, clinical, histopathological, and pathophysiological studies have implicated that delayed arterial healing and poor re-endothelialization may play a major role in the pathogenesis of LST. * 那么血管内皮细胞到底有哪些功能呢？ * 血管内皮细胞是一层连续覆盖整个血管腔表面的扁平细胞，内衬于血管内壁。正常状态下，内皮细胞产生多种血管活性物质，以维持血管的正常活动。 血管内皮细胞分泌大量的舒血管和缩血管物质，以维持血管的正常功能，但是在众多分泌的物质中，NO是一种重要的血管活性物质。那么NO为什么如此重要呢？ * NO可以抑制血管内血小板的聚集和白细胞的激活，保持血管平滑肌细胞处于非增增殖状态，另外还可以使血管平滑肌保持一定的张力，同时，NO也可以抑制缩血管物质血管紧张素II和内皮缩血管肽的活性。NO活性或生物利用度下降或内皮产生的舒缩血管物质失衡是导致内皮功能紊乱的关键原因。 Nitric oxide (NO), a key factor generated by ECs, is associated with inhibition of platelet and leukocyte activation, and maintenance of vascular smooth muscle in a nonproliferative state. In addition to being the main determinant of basal vascular smooth muscle tone, NO opposes the actions of potent endothelium-derived contracting factors such as angiotensin-II and endothelin(ET)-1 (15–18). Impairment of NO bioactivity or bioavailability and/or imbalance between endothelium-derived relaxing and contracting factors is crucial in the mechanisms of endothelial dysfunc