CELLULAR BIOLOGY OF HUMAN INTIMAL HYPERPLASTIC STENOSIS

被引:33
作者
CHAN, P
MUNRO, E
PATEL, M
BETTERIDGE, L
SCHACHTER, M
SEVER, P
WOLFE, J
机构
[1] Department of Vascular Surgery, St Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, London
[2] Department of Clinical Pharmacology, St Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, London
来源
EUROPEAN JOURNAL OF VASCULAR SURGERY | 1993年 / 7卷 / 02期
关键词
VASCULAR SMOOTH MUSCLE; HEPARIN; CELL CULTURE; RESTENOSIS; INTIMAL HYPERPLASIA;
D O I
10.1016/S0950-821X(05)80752-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Restenosis after angioplasty and vascular surgery remains a major unsolved clinical problem. Vascular smooth muscle cell (VSMC) hyperplasia is an invariable response, but in 20-50% of cases proceeds to compromise the vessel lumen. We sought to identify cellular characteristics of human VSMC which are associated with restenosis. Human VSMC were grown from 135 samples of vascular tissue derived from patients undergoing primary cardiovascular surgery and revision surgery for restenosis. Cells derived from normal vein and artery, atherosclerotic plaques and from stenotic lesions were studied for successful proliferation in cell culture. Furthermore, growth rates were measured in response to 15% foetal calf serum ± inhibition with heparin (100 μg/ml). Significantly fewer cells from atherosclerotic plaques progress to the third passage in cell culture than those derived from stenoses and controls (p < 0.001, Chi square) and growth rates after the third passage could not be studied in these cells. Of cells that progress to this stage, growth rates do not differ between stenosis-derived and normal cells under standard conditions. VSMC from mature atherosclerotic plaques may have undergone senescent changes. Stenosis-derived cells do not grow more rapidly than normal cells, but are significantly less sensitive to heparin (p < 0.001, Mann-Witney test), which is a major physiological inhibitor of VSMC growth. Differences in biological characteristics of human VSMC, observed in cell culture, may provide important insights into human vascular disease. © 1993 Grune & Stratton Ltd.
引用
收藏
页码:129 / 135
页数:7
相关论文
共 28 条
[1]  
Ross, The pathogenesis of atherosclerosis-an update, N Engl J Med, 314, pp. 488-498, (1986)
[2]  
Taylor, Wolfe, Tyrrell, Mansfield, Nicolaides, Houston, Graft stenosis: justification for one year surveillance, Br J Surg, 77, pp. 1125-1128, (1990)
[3]  
McBride, Lange, Hillis, Restenosis after successful coronary angioplasty, N Engl J Med, 318, pp. 1734-1737, (1988)
[4]  
McCollum, Alexander, Kenchington, Franks, Greenhalgh, Antiplatelet drugs in femoropopliteal vein bypasses: a multicentral trial, J Vasc Surg, 13, pp. 150-162, (1991)
[5]  
Chesebro, Fuster, Elveback, Et al., Effect of dipyridamole and aspirin on late vein graft patency after coronary artery bypass operations, N Engl J Med, 310, pp. 209-214, (1984)
[6]  
Kretchsmer, Schemper, Ehringer, Et al., Influence of postoperative anticoagulant treatment on patient survival after femoropopliteal vein bypass surgery, Lancet, 1, pp. 797-798, (1988)
[7]  
Veith, Gupta, Ascer, Et al., Six year prospective multi-centre randomised comparison of autologous saphenous vein and expanded PTFE in infra-inguinal arterial reconstruction, J Vasc Surg, 3, pp. 104-114, (1986)
[8]  
Kohler, Kirkman, Clowes, Effect of heparin on adaptation of vein grafts to the arterial circulation, Arteriosclerosis, 9, pp. S23-S28, (1989)
[9]  
Ip, Fuster, Israel, Badimon, Badimon, Chesebro, The role of platelets, thrombin and hyperplasia in restenosis after coronary angioplasty, Journal of the American College of Cardiology, 17, pp. 77B-88B, (1991)
[10]  
Schwartz, Bourassa, Lesperance, Et al., Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty, N Engl J Med, 318, pp. 1714-1719, (1988)