Painter T A
Division of Vascular Surgery, Northwestern University, Chicago, Illinois.
Artif Organs. 1991 Apr;15(2):103-18. doi: 10.1111/j.1525-1594.1991.tb00768.x.
Arterial wall injury either by balloon catheter, drying, or scraping results in a denudation of endothelial cells (EC) and a subsequent proliferation of smooth-muscle cells (SMC). The degree of SMC proliferation appears to be dependent on the degree of initial injury and not to the loss of the overlying endothelium. Successful reendothelialization of denuded areas depends on the size of the denuded segment as well as SMC-EC interactions. Prolonged exposure of SMC to serum substances results in inhibition of EC regrowth, the production of prostacyclin by SMC, and the development of a thromboresistant surface. Heparin appears to inhibit SMC proliferation in vivo (as well as in vitro), an effect that is independent of platelet SMC interaction. EC-derived heparin in vivo may also result in inhibition of SMC proliferation. Platelets may play an important role in the early response to arterial injury and development of myointimal hyperplasia (MIH), but their long-term role appears to be minor. Antiplatelet agents have widely varying species-dependent effects on platelets and platelet-vessel wall interactions, but in specific circumstances they may inhibit MIH. The precise role of steroid drugs and immunosuppression on MIH in arterial injury models awaits further study. The role of lipoproteins in MIH is unclear; however, the inhibition of MIH by omega-3 fatty acids in vivo as well as their inhibition of platelet-derived growth factor production by EC in vitro implies a regulatory role. Acute hypertension results in a marked proliferation of EC and SMC in vivo and enhances the proliferative response to injury as well. Low wall shear stress, turbulence, and boundary layer separation all increase EC turnover, a likely influence on EC growth factor production. The compliance mismatch resulting from graft-artery anastomoses, injury, and endarterectomy results in locally increased cyclical stretch, which may predispose to SMC proliferation.
球囊导管、干燥或刮擦等造成的动脉壁损伤会导致内皮细胞（EC）剥脱，随后平滑肌细胞（SMC）增殖。SMC增殖的程度似乎取决于初始损伤的程度，而非取决于覆盖其上的内皮的缺失。剥脱区域成功的再内皮化取决于剥脱节段的大小以及SMC与EC的相互作用。SMC长时间暴露于血清物质会导致EC再生受到抑制、SMC产生前列环素以及形成抗血栓表面。肝素似乎在体内（以及体外）抑制SMC增殖，这种作用独立于血小板与SMC的相互作用。体内EC衍生的肝素也可能导致SMC增殖受到抑制。血小板可能在对动脉损伤的早期反应和肌内膜增生（MIH）的发展中起重要作用，但其长期作用似乎较小。抗血小板药物对血小板及血小板与血管壁相互作用具有广泛不同的物种依赖性效应，但在特定情况下它们可能抑制MIH。类固醇药物和免疫抑制对动脉损伤模型中MIH的确切作用有待进一步研究。脂蛋白在MIH中的作用尚不清楚；然而，ω-3脂肪酸在体内对MIH的抑制作用以及它们在体外对EC产生血小板衍生生长因子的抑制作用意味着其具有调节作用。急性高血压会导致体内EC和SMC显著增殖，并增强对损伤的增殖反应。低壁面剪应力、湍流和边界层分离都会增加EC更新，这可能影响EC生长因子的产生。移植动脉吻合、损伤和动脉内膜切除所导致的顺应性不匹配会使局部周期性拉伸增加，这可能易引发SMC增殖。
