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《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:

2009年第1期

页码:

38-40

栏目:

基础研究

出版日期:

2009-02-28

文章信息/Info

Title:

Effect of bisoprolol on heart function of anti-β1-adrenoceptor autoantibody-positive rats with heart failure

作者:

马利祥¹; 杨新春²; 王树岩²; 张智勇²; 刘秀兰²

1.秦皇岛市第一医院心内科，河北 秦皇岛 066000； 2.首都医科大学附属北京朝阳医院心脏中心，北京 100020

Author(s):

MA Li-xiang¹;  YANG Xin-chun²;  WANG Shu-yan²;  ZHANG Zhi-yong²;  LIU Xiu-lan²

1.Department of Cardiology, First Hospital of Qinhuangdao， Qinhuangdao 066000, Hebei, China; 2.Cardiologic Center, Beijing Chaoyang Hospital-Affiliated to Capital University of Medical Sciences, Beijing 100020, China

关键词:

比索洛尔; 心力衰竭; 肾上腺素能β1受体; 自身抗体; 大鼠

Keywords:

bisoprolol heart failure;  β1-adrenoceptor;  autoantibody;  rat

分类号:

Q577；R541

DOI:

-

文献标识码:

A

摘要:

目的 探讨比索洛尔对抗β1-肾上腺素能受体（β1-AR）自身抗体阳性心衰大鼠心功能的影响。方法 采用缩窄腹主动脉的方法，建立慢性心力衰竭的大鼠模型。将心衰组大鼠（90只最终入组65只）随机分为心衰治疗组（40只）和心衰非治疗组（25只）。心衰治疗组接受比索洛尔4周的治疗。心衰非治疗组接受同剂量的蒸馏水同样时间的治疗。应用ELISA法检测大鼠血清β1-AR自身抗体的阳性率和滴度；应用BL-420E生物机能实验系统于治疗前及治疗后4周检测心功能。结果 ①治疗组组内抗β1-AR自身抗体阳性者较阴性者左室舒张末压低，左室变化的最大速率升高，但无统计学意义;非治疗组组内抗β1-AR自身抗体阳性者较阴性大鼠的心功能进一步恶化，左室舒张末压明显升高（P<0.01），左室变化的最大速率下降（P<0.05）。②治疗组中抗β1-AR自身抗体阳性者与非治疗组中抗β1-AR自身抗体阳性者比较,前者较后者左室舒张末压明显下降（P<0.01）；左室变化的最大速率均显著升高（P<0.05）。结论 比索洛尔治疗后，心衰大鼠抗β1-AR自身抗体阳性者的心功能较非治疗组中抗β1-AR自身抗体阳性者的心功能明显改善。同为治疗组的抗β1-AR自身抗体阳性者的心功能较阴性者的左室舒张末压低，左室变化的最大速率升高。

Abstract:

AIM To explore the effect of bisoprolol on anti-β1-adrenoceptor (β1-AR) autoantibody-positive rats with heart failure. METHODS A model of SD rats with heart failure was established by constricting the abdominal aorta. The rats were randomly divided into two groups: 40 rats in bisoprolol treatment group and 25 rats in no bisoprolol treatment group. The positive rate and the titer of serum anti-β1-AR autoantibody were detected by ELISA. The heart function before and 4 weeks after treatment was examined by biofunctional system. RESULTS ①In bisoprolo treatment group, left ventricular end diastolic pressure (LVEDP) of the anti-β1-AR autoantibody-positive rats was lower than that of autoantibody-negative rats and the speed of left ventricular dp/dtmax of the anti-β1-AR autoantibody-positive rats was higher than that of autoantibody-negative rats, with no significant difference. In no bisoprolo treatment group, heart function of autoantibody-positive rats was worse than that of anti-β1-AR autoantibody-negative rats. Their LVEDP increased (P<0.01) and left ventricular dp/dtmax decreased (P<0.05). ②LVEDP of anti-β1-AR autoantibody-positive rats with heart failure in bisoprolol treatment group was lower than that of anti-β1-AR autoantibody-positive rats in no bisoprolol treatment group and their left ventricular dp/dtmax increased obviously (P<0.05). CONCLUSIONS After bisoprolol treatment, the heart function of anti-β1-AR autoantibody-positive rats with heart failure in bisoprolol treatment group is more obviously improved than that of anti-β1-AR autoantibody- positive rats in no bisoprolol treatment group. In bisoprolol treatment group, LVEDP of anti-β1-AR autoantibody-positive rats with heart failure is lower and left ventricular dp/dtmax is higher, compared with those autoantibody-negative rats.

参考文献/References

[1］ Dalla Libera L, Ravara B, Gobbo V, et al. Skeletal muscle myofibrillar protein oxidation in heart failure and the protective effect of carvedilol［J］. J Mol Cell Cardiol, 2005, 38(5):803-807.
［2］ Jahns R, Boivin V, Siegmund C, et al. autoantibodies activating human β1-adrenergic receptors are associated with reduced cardiac function in chronic heart failure［J］. Circulation, 1999, 99(5):649-654.
［3］ Magnusson Y, Wallukat G, Waagstein F, et al. Autoimmunith in idiopathic dilated cardiomyopathy. Characterization of antibodies against the β1-adrenoceptor with positive chronotropic effect［J］. Circulation, 1994, 89(6):2760-2767.
［4］ Wallaukat G， Müller J, Podlowski S, et al. Agonist-like beta-adrenoceptor antibodies in heart failure［J］. Am J Cardiol, 1999, 83(12A):75H-79H.
［5］ Liu X, Callaerts-Vegh Z, Evans KL, et al. Chronic infusion of beta-adrenoceptor antagonist and inverse agonists decrease elevated protein kinase a activity in transgenic mice with cardiac-specific over expression of human beta2-adrenoceptor［J］. J Cardiovasc Phamacol, 2002, 40(3):448-455.
［6］ Liu HR, Zhao RR, Jiao XY, et al. Relationship of myocardial remodeling to the genesis of serum autoantibodies to cardiac beta1-adrenoceptors and muscarinic type 2 acetylcholine receptors in rats［J］. J Am Coll Cardiol, 2002, 39(11):1866-187.
［7］ Jahns R, Boivin V, Krapf T, et al. Modulation of beta1-adrenoceptor activity by domain-specific antibodies and heart failure-associated autoantibodies［J］. J Am Coll Cardiol, 2000, 36(4):1280-1287.
［8］ 李慧丽,王彬尧，张峰,等. 一种慢性心力衰竭模型的建立［J］. 心脏杂志, 2004, 16 (3):287.
［9］ Miao GB, Liu JC, Liu MB, et al. Autoantibody against β1-adrenergic receptor and left ventricular emodeling changes in response to metoprolol treatment［J］. Eur Clinical Investigation, 2006, 36(9):614-620.

备注/Memo

备注/Memo:

收稿日期：2007-11-23.通讯作者：杨新春，主任医师，主要从事冠心病、心力衰竭及介入心脏病学研究Email:yangxc@medmail.com.cn 作者简介：马利祥，主治医师，硕士生Email:mlx99999@sohu.com

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更新日期/Last Update: 2009-04-02