Bassenge E
Institute of Applied Physiology, University of Freiburg, F.R.G.
Eur Heart J. 1989 Nov;10 Suppl F:22-7. doi: 10.1093/eurheartj/10.suppl_f.22.
Large coronary artery calibres are regulated by humoral factors (autacoids) released from the endothelial cell lining. Several hormones, transmitters and platelet-derived products like serotonin and ATP or acetylcholine, noradrenaline, and histamine, stimulate such an autacoid release and thus an endothelium-mediated dilation in addition to their direct constrictor effect on the vasculature. Another mechanical stimulus is the flow-induced shear stress acting as viscous drag upon the endothelial surface along with the pulsatile stretching of the endothelial lining, which causes, in a moment to moment fashion, a continuous adjustment of coronary calibres. With endothelial function impaired or absent as in atheromatosis or after balloon catheter denudation this adjustment is compromised. Thus unbalanced constrictor effects may become effective especially in the presence of a simultaneously reduced platelet antiaggregation.
大冠状动脉口径受内皮细胞层释放的体液因子(自分泌物质)调节。几种激素、递质以及血小板衍生产物,如血清素、三磷酸腺苷、乙酰胆碱、去甲肾上腺素和组胺,除了对血管系统有直接收缩作用外,还会刺激此类自分泌物质释放,进而引起内皮介导的血管舒张。另一种机械刺激是血流诱导的剪切应力,它如同粘性阻力作用于内皮表面,同时伴随着内皮细胞层的搏动性拉伸,这使得冠状动脉口径时刻都在持续调整。在动脉粥样硬化或球囊导管剥脱术后,当内皮功能受损或缺失时,这种调节就会受到影响。因此,特别是在血小板抗聚集同时降低的情况下,不平衡的收缩效应可能会起作用。