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|本期目录/Table of Contents|

卡维地洛对心功能不全患者神经激素系统的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2007年第6期
页码:
669-671/674
栏目:
临床研究
出版日期:
2007-12-20

文章信息/Info

Title:
Carvedilol regulation of neurohormone system in patients with congestive heart failure
作者:
杨永健张鑫 杨大春速晓华
成都军区总医院心血管内科,四川 成都 610083
Author(s):
YANG Yong-jian ZHANG Xin YANG Da-chun SU Xiao-hua
Department of Cardiology, General Hospital, Chengdu Military Area Command, Chengdu 610083, Sichuan, China
关键词:
卡维地洛心力衰竭 充血性受体肾上腺素能
Keywords:
carvedilol heart failurecongestive receptors adrenergic
分类号:
R541.2
DOI:
-
文献标识码:
A
摘要:
目的 探讨卡维地洛对慢性心功能不全患者神经激素及肾上腺素受体β1、β2、α1自身抗体的影响。方法 60例慢性心功能不全患者随机分为卡维地洛组(36例)和常规治疗组(24例)。常规治疗组应用血管紧张素转换酶抑制剂、利尿剂和洋地黄制剂。卡维地洛组在此基础上加用卡维地洛。随访半年,超声心动图测定心功能参数,检测血浆去甲肾上腺素(NE)、肾素(PRA)、血管紧张素II(Ang II)、醛固酮(ALD)、及对抗心脏β1、β2、α1自身抗体。结果 治疗后,卡维地洛组左室舒张末内径和收缩末内径分别为(57±6)mm和(43±6)mm显著低于常规治疗组的(64±5)mm和(52±5)mm(均P<0.01);左室射血分数为(51±8)% ,显著高于常规治疗组的(42±6)%(P<0.01)。治疗后卡维地洛组血浆NE、PRA、Ang II、ALD、3种抗体滴度均显著降低(均P<0.01),且卡维地洛组血浆NE、PRA、Ang II、ALD水平、3种抗体滴度也显著低于常规治疗组,差异有统计学意义(P<0.05)。结论 卡维地洛通过阻断神经激素激活及降低心衰患者心脏自身β1、β2、α1受体抗体水平而改善心功能。
Abstract:
AIM To investigate the effect of Carvedilol on cardiac function, neurohormone and autoantibodies against cardiac β1, β2 and α1 adrenergic receptors in patients with congestive heart failure (CHF). METHODS Sixty patients with CHF were randomly divided into two groups: conventional group treated with ACE inhibitor, digoxin and diuretic and Carvedilol group treated with Carvedilol on the basis of the conventional treatment. Patients were followed up for six months, during which cardiac function parameters were measured by echocardiography and serum levels of neorphinephrine (NE), angiotensionII(Ang II), aldosterone (ALD), plasm renin activity (PRA), β1, β2 and α1 adrenergic receptors were detected respectively. RESULTS After Carvedilol treatment, left ventricular enddiastolic diameter (57±6)mm and left ventricular endsystolic diameter (43±6)mm were smaller than those (64±5) mm and (52±5 mm) in conventional group, while left ventricular ejection fraction [(51±8)%] was higher than that [(42±6)%] in conventional group(P<0.01). Carvedilol group had a significant increase in plasma concentrations of NE, ALD, AngIIand PRA compared with those in control (P<0.01). The titers of autoantibodies against cardiac β1, β2 and α1 adrenergic receptors all significantly decreased compared with those of pretreatment in Carvedilol group (P<0.01) and they were lower than those in conventional group(P<0.01). CONCLUSION Neurohormon and β1, β2 and α1 adrenergic receptors are involved in the process of pathophysiology and development of CHF. Carvedilol can inhibit this process and improve cardiac function by neurohormon inhibition of β1, β2 and α1 adrenergic receptors in patients with congestive heart failure.

参考文献/References

[1] Chobanian AV, Bakris GL, Black HR,et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report [J]. JAMA,2003, 289(19),2560-2572.

[2] Tan LB, Schlosshan D, Barker D. Fiftieth anniversary of aldstone:from discovery to cardiovascular therapy[J]. Int J Cardiol,2004,96(3):321-333.

[3] 张麟,胡大一,史旭波,等. 心脏β1和M2受体自身抗体与心力衰竭的研究[J]. 中华内科杂志,2001,40(7):445-447.

[4] Podlowski S,Luther HP,Morwinski R, et al.Agonistic anti-β1adrenergic receptor autoantibodies from cardiomyopathy patients reduce theβ1adrenergic receptor expression in neonatal rat cardiomyocytes[J]. Circulation,1998, 98(22): 2470-2476.

[5] Luther HP, Houmth V,Wallukat G. Alpha 1 adrenergic receptor antibodies in patients with primary hypertension[J]. Hypertension,1997,29(2):678-682.

[6] Yao A, Kohmoto O, Oyama T, et al.Characteristic effects of alphalbeta1, 2adrenergic blocking agent,carvedilol,on [Ca2+] in ventricular myocytes compared with those of timolol and atenolol[J]. Circ J,2003 ,67(1):83-90.

[7] Liu X ,CallaertsVegh Z,Evans KL, et al.Chronic infusion of betaadrrenoceptor antagonist and inverst agnoists decrease elevated protein kinase a activity in transgenic mice with cardiacspecific overexpression of human peta 2adrenoceptor[J]. J Cardiovasc Pharmacol,2002,40(5):448-455.

备注/Memo

备注/Memo:
收稿日期:2006-12-06.作者简介:杨永健,博士, 副主任医师 Email:yangyongjian38@yahoo.com
更新日期/Last Update: