Chan P, Patel M, Betteridge L, Munro E, Schachter M, Wolfe J, Sever P
Department of Clinical Pharmacology, St Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, London, UK.
Lancet. 1993 Feb 6;341(8841):341-2. doi: 10.1016/0140-6736(93)90139-8.
Proliferation of vascular smooth muscle cells (VSMC) underlies myointimal hyperplasia, which can lead to restenosis after angioplasty and vascular surgery. We propose that some individuals have an intrinsic capacity for this exaggerated response to vascular injury, partly through decreased sensitivity to the physiological growth inhibitor heparin. We investigated the effect of heparin on VSMC from restenotic lesions and from apparently normal vessels of the same patients, and VSMC from control patients undergoing primary bypass procedures. Cells from patients with restenosis (both restenotic lesion and undiseased vein) showed much lower sensitivity to growth inhibition by heparin than the controls (median inhibition 8 [95% Cl -2 to 25] vs 22 [15-44]%, p < 0.001); this finding suggests aberrant growth regulation in these cells.
血管平滑肌细胞(VSMC)的增殖是肌内膜增生的基础,而肌内膜增生可导致血管成形术和血管手术后的再狭窄。我们认为,部分个体对血管损伤存在这种过度反应的内在能力,部分原因是对生理性生长抑制剂肝素的敏感性降低。我们研究了肝素对同一患者再狭窄病变处和看似正常血管的VSMC以及接受初次搭桥手术的对照患者的VSMC的影响。再狭窄患者(包括再狭窄病变处和未患病静脉)的细胞对肝素生长抑制的敏感性远低于对照组(中位抑制率8 [95%可信区间 -2至25]% 对22 [15 - 44]%,p < 0.001);这一发现表明这些细胞的生长调节异常。