缓激肽在依那普利干预心肌梗塞大鼠心肌胶原代谢中的作用  

Effects of bradykinin on collagen from rat heart after myocardial infarction

作　　者：张海柱[1] 雷立权[2] 崔长琮[1] 黄英[3] 

机构地区：[1]西安交通大学第一医院心内科,成都610041 [2]西安交通大学医学院病理生理学教研室,西安710061 [3]四川大学医学院病理生理教研室,成都610041

出　　处：《西安交通大学学报（医学版）》2002年第4期384-386,共3页Journal of Xi’an Jiaotong University（Medical Sciences）

摘　　要：目的　探讨缓激肽 (BK)对大鼠心肌梗塞 (MI)后心肌胶原生化改建的影响 ,以及血管紧张素转换酶抑制剂 (ACEI)对心肌胶原的影响是否与抑制BK的降解有关。方法　复制大鼠MI模型后 ,第 3天开始给予依那普利(5 0 0 μg·kg-1·d-1) 4周 ,测定左心室非梗塞区组织的胶原含量及Ⅰ、Ⅲ型胶原的比值 (Ⅰ /Ⅲ ) ,并与依那普利 +BKB2 受体阻断剂HOE 14 0 (5 0 0 μg·kg-1·d-1由微渗透泵给入 )组、血管紧张素ⅡⅠ型受体 (AT1)阻断剂Losartan(3mg·kg-1·d-1)组及对照组相比较。结果　依那普利、Losartan组的胶原含量及其Ⅰ /Ⅲ比值均较对照组降低(P <0 0 5 ) ,而Losartan组的胶原含量及其Ⅰ /Ⅲ比值又低于依那普利组 (P <0 0 5 ) ,依那普利 +HOE 14 0组的胶原含量及Ⅰ /Ⅲ比值较单独用依那普利组明显升高 (P <0 0 5 )。结论　BK能抑制大鼠MI后左心室胶原的生成及降低胶原Ⅰ /Ⅲ比值 ;ACEI阻抑左心室胶原生化改建的作用机制是既抑制了血管紧张素Ⅱ (AngⅡ )的生成又促使了心肌局部BK的积累。Objective To investigate the effects of bradykinin (BK) on collagen from rat heart after myocardial infarction and the importance of BK in ACEI therapy in rats after myocardial infarction. Methods We compared the effects of enalapril (500?μg·kg -1 ·d -1 ),enalapril (500?μg·kg -1 ·d -1 )with BKB 2 receptor antagonist (HOE 140 500?μg·kg -1 ·d -1 ), losartan (3?mg·kg -1 ·d -1 ) on collagen content and the ratio of type Ⅰ to type Ⅲ collagen (Ⅰ/Ⅲ) of noinfarcted area after myocardial infarction in rats. The treatment continued for 4 weeks.Results Enalapril reduced the collagen content and Ⅰ/Ⅲ compared with the untreated MI group ( P <0.05), and these effects of enalapril were partly blunted by concomitant treatment with HOE 140 ( P <0.05). Losartan was less effective than enalapril ( P < 0.05 ). Conclusion BK can reduce collagen content and Ⅰ/Ⅲ of the infarcted heart of rat. The effects of ACEI are due to both blockade of Ang Ⅱ formation and inhibition of BK degradation.

关 键 词：缓激肽 依那普利 干预 心肌梗塞 大鼠 心肌胶原代谢 

分 类 号：R542.22[医药卫生—心血管疾病]