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血管紧张素转换酶抑制剂对心脏移植后冠状血管增殖病变的影响 被引量:2

Effect of ACEI on proliferative coronary disease after heart transplantation
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摘要 目的通过建立大鼠心脏移植后冠状血管增殖病变的模型,观察血管紧张素转换酶抑制剂(ACEI)对心脏移植后冠状血管增殖病变的影响。方法设立对照组、结扎组、ACEI+结扎组,观察2周后各组大鼠血液、心肌AngⅡ含量,心肌AngⅡ受体密度,及血管病理学结果。结果各组血液AngⅡ含量差异无统计学意义,结扎组心肌AngⅡ含量明显增高(17.42±5.49)fmol/mg.蛋白P<0.001比对照组,ACEI+结扎组AngⅡ含量明显下降(5.35±1.95)fmol/mg。蛋白P< 0.01比结扎组,结扎组AngⅡ受体密度增高(48.80±4.32)fmol/mg蛋白P<0.01比对照组,ACEI +结扎组内膜增生比结扎组明显减轻[内膜厚度(21.01±4.55)μm比(60.34±9.32)μm,P< 0.01)。结论心脏局部肾素-血管紧张素系统,AngⅡ及AngⅡ受体参与移植后冠状血管病变,A- CEI明显抑制移植后冠状血管病增殖变。 Objective To study the effect of ACEI on proliferative coronary artery disease after heart transplantation. Methods Posttransplantation rats were randomly divided into 3 groups: control group,ligation group and ACEI plus ligation group (ACEI group). In the 3 groups, changes of Ang Ⅱ contents in plasma and myocardium, density of Ang Ⅱ receptor in myocardium and vascular pathological results were observed. Results There was no significant difference in the contents of plasma Ang Ⅱ among the three groups. The content of myocardial Ang Ⅱ in ligation group was 17.42 ± 5.49 fmol/mg protein, which was significantly higher than in control group (P 〈 0.01 ), and that in ACEI group was 5.35 ± 1.95 fmol/mg protein, which was significantly lower than in ligation group ( P〈 0.01 ). The density of Ang Ⅱ receptor in ligation group was 48.80 ± 4.32 fmol/mg protein,which was significantly higher than in control group ( P 〈0.01 ). Vessel intimal thickness in ACEI group was significantly less than in ligation group (21 . 01 ± 4.55 μm vs 60.34 ± 9.32 μm,P〈 0.01) , Conclusion The heart regional RAS system and Ang Ⅱ and Ang Ⅱ receptor are involved in the proliferative coronary disease after heart transplantation. ACEI can inhibit significantly the intimal hyperplasia of coronary artery after heart transplantation.
作者 韩振 夏求明
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2006年第12期1478-1480,共3页 Chinese Journal of Experimental Surgery
关键词 ACEI AngⅡ 心脏移植 冠状血管病 ACEI Angiotensin Ⅱ Heart transplantation Coronary artery disease
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参考文献6

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共引文献33

同被引文献22

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