多粘菌素B+维拉帕米抑制内膜增生的实验研究Experimental study of polymyxin B++verapamil on the intimal proliferation in rabbit
周晓阳,王瑞英,任江华,卢宏彪
摘要(Abstract)：
目的 探讨血管成行术后再狭窄的预防。方法 以兔右颈总动脉内膜剥脱为实验模型，３０只兔随机分为单纯损伤组（ｎ＝ １２）、损伤＋ 药物治疗组（简称药物治疗组，ｎ＝ １２）和假手术组（ｎ＝ ６），术后１４ 天行病理形态学观察及增殖细胞核抗原（Ｐｒｏｌｉｆｅｒａｔｉｎｇ ｃｅｌｌｎｕｃｌｅａｒ ａｎｔｉｇｅｎ，ＰＣＮＡ）免疫组化分析。结果 药物治疗组右颈总动脉内膜平均厚度显著小于单纯损伤组（３５．８１±１６．１３ μｍ ｖｓ ７２．１４±１４．６６μｍ ，Ｐ＜ ０．０１）；药物治疗组右颈总动脉狭窄度显著小于单纯损伤组（２１．７４％ ±８．９９％ ｖｓ ５３．６８％ ±１５．５７％ ，Ｐ＜ ０．０１）；药物治疗组细胞增殖指数显著小于单纯损伤组（０．２３０±０．０４７ ｖｓ ０．４２９±０．０５５，Ｐ＜ ０．０１）。结论 蛋白激酶Ｃ（ｐｒｏｔｅｉｎ ｋｉｎａｓｅ Ｃ，ＰＫＣ）特异抑制剂多粘菌素Ｂ联用Ｃａ２＋ 通道阻滞剂维拉帕米能有效抑制受损血管内膜增生，对预防再狭窄可能具有潜在临床应用前景
关键词(KeyWords)： 蛋白激酶C;多粘菌素B;增殖细胞核抗原;内膜增生;维拉帕米
基金项目(Foundation):
作者(Author): 周晓阳,王瑞英,任江华,卢宏彪
参考文献(References)：
- 1 ForresterJS, Fishbein M,HelfantR, etal. Aparadigmfor restenosisbased on cellbiology: cluesforthe devel-opm ent ofnew preventive therapy. JAm CollCardiol,1991,17:758.
- 2 Newby AC, George SJ. Proposed roles for growth fac-tors in m ediating sm ooth m uscles proliferation in vascu-lar pathologies. Cardiovascular Research, 1993, 27:1173.
- 3 Clowes AW, Reidy MA, ClowesMM.Kineticsofcellu-ar proliferation after arterialinjury Ⅰ. Sm ooth m usclegrow th in the absence of endothelium . Lab Invest,1989,49:327.
- 4 Bravo R, Frank R, BlundellPA, etal. Cyclin/PCNAisthe auxilliary protein of DNA polyerase-delta. Nature(Lond), 1987,326:515.
- 5 RalesN, BoisselJP. Growth-stim ulating effectofcate-cholam ine on rataorta sm ooth m uscle cells in culture. Jcellphysiol, 1983,116:167.
- 6 Zhang Y, Cincotta AH. Inhibitory effectsofbrom ocrip-tine on vascular sm ooth m uscle cell proliferation.Atherosclerosis, 1997,133:37.
- 7 Macleod DC,StraussC,Escaned M,etal. Proliferationand extracelluarm atrix synthesis as sm ooth m usclecellscultured from hum an coronary atherosclerotic andrestenosis lesion. JAm CollCardiol, 1994,23:59.
- 8 赵世军,张瑞英,王岚峰,等.口服维拉帕米的抗凝作用:抑制血小板膜糖蛋白Ⅱb/Ⅲa受体与血小板功能.哈尔滨医科大学学报,1996,(1):40.
- 9 陈日炎,江黎明,覃燕梅,等。蛋白激酶C在血小板聚集中的作用.生物化学杂志,1995,(4):467