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镍钛自膨胀支架置入血管后细胞凋亡与增生的实验观察 被引量:1

Experimental observation on apoptosis and proliferation of smooth muscle cells after implantation of NITI self-expanding stent
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摘要 目的 血管内支架置入后的再狭窄是尚未解决的主要课题 ,本研究对置入镍钛 (NITI)自膨胀支架的动物进行研究 ,观察支架置入后血管平滑肌细胞 (VSMC)的凋亡与增生的关系 ,为再狭窄的防治提供新的方法。方法 在兔的腹主动脉内置入 30个NITI合金自膨胀支架 ,按不同时间处死动物 ,采用电镜和 3′ 末端DNA原位标记法 (TUNEL)观察VSMC的凋亡。结果 从支架置入后的 2 4h到 8周 ,支架置入部位均可见到凋亡的VSMC ,3~ 6周时 ,凋亡达到高峰 ,8周以后凋亡细胞开始减少。凋亡的细胞主要分布于血管的新生内膜层 ,但中膜层也存在有少量的凋亡细胞。结论 NITI自膨胀支架置入后 ,不仅有SMC的增生 ,也有SMC的凋亡。 Objective Stent implantation is the most important achievement in the therapy of cardiovascular diseases.Stent can prevent restenosis,but it can not reduce the proliferation of smooth muscle cells.Now,most methods of treating restenosis aim at inhibiting proliferation of SMCs.The objective of the present study was to observe the effects of apoptosis on the restenosis after stenting.Methods 30 rabbits were studied and 30 NITI stents were implanted in the normal abdominal aorta.TUNEL and electron microscope were used to examine the apoptosis cells.Results Apoptosis cells appeared in the wall of stenting segment from 24hr to 8 weeks after implantation of the stent,with the peak of apoptosis between 3-6 weeks,while the new intima was formed completely and covered by a single layer of cells-endotheliocyte.The apoptosis cells were distributed in both new intima and media.Conclusion After implantation of stent,the SMCS not only proliferate but also die (apoptosis),which may play an important role in maintaining the number of SMCs.Increase in apoptosis cells may reduce restenosis after stenting.
出处 《中华老年心脑血管病杂志》 CAS 2000年第4期256-258,共3页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词 凋亡 平滑肌细胞 镍钛支架 apoptosis smooth muscle cells NI TI stent
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  • 1Bennett MR, Gibson DF, Schwartz SM et al. Binding and phagocytosis of apoptotic vascular smooth muscle cells is mediated in part by exposure of phosphatidylserine [ J ]. Circ Res,1995,77: 1136- 1140.
  • 2Kockx MM, Knaapen MW. The role of apoptosis in vascular disease[J], J Pathol,2000, 190:267 - 280.
  • 3Bennett MR, Evan GI, Schwartz SM et al. Apoptosis of human vascular and coronary atherosclerotic plaques[J]. J Clin Invest,1995,95,2266 - 2274.
  • 4Han DK, Haudenschild CC, Hong MK et al. Evidence for apoptosis in human atherogenesis and in a rat vascular injury model[J]. Am J Pathol, 1995,147:267 - 277.
  • 5Tanaka M, ho H, Adachi S et al. Hypoxia induces apoptosis with enhanced expression of Fas antigen messenger RNA in cultured neonatal rat cardiomyocytes [J]. Circ Res, 1994, 75 :426 - 433.
  • 6Gofflieb RA, Burleson RO, Kloner RA et al, Reperfusion injury induced apoptosis in rabbit cardiom ocytes[J], J Clin Invest,1994,94:1621 - 1628.
  • 7Bennett MR, Evan GI, Newby AC. Deregulated expression of the c-myc oncogene abolishes inhibition of proliferation of rat gamma heparin and cyclic nucleotide analogues and induces apoptosis[J]. Circ Res, 1994,74:525 - 536.
  • 8Bochaton-Piallat ML, Gabbiani F, Redard M et al, Apoptosis participates in cellularity regulation during rat aortic intimal thickening[J]. Am J Pathology, 1995, 146:1059 - 1064.
  • 9Kollum M, Kaiser S, Kinscherf R et al. Apoptosis after stent implantation compared with balloon angioplasty in rabbits. Role of macrophages[J], Arterioscler Thromb Vasc Biol, 1997, 17 :2383 - 2388.
  • 10Isner JM, Keraney M, Bortmam S et al. Apoptosis in human atherosclerosis and restenosis[J]. Circulation, 1995,91:2703 -2711.

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