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胶原纤维增生对慢性心力衰竭的影响及氯沙坦钾的干预作用 被引量:42

Effect of collagen prolieration and losartan on chronic heart failure
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摘要 目的:探讨血清Ⅰ型前胶原羧基端肽(P Ⅰ P)和Ⅲ型前胶原氨基端肽(PⅢP)与心衰和心室重构的关系,同时观察氯沙坦钾的干预作用。方法:将40例慢性心衰患者随机分为常规治疗组和氯沙坦钾组(每天口服氯沙坦钾50mg)。20例无心脑血管和肝脏疾病者设为对照组。所有患者于治疗前采用放射免疫分析法测定P Ⅰ P、PⅢP、血管紧张素Ⅱ(AngⅡ)、醛固酮,超声心动图测定室间隔厚度(IVST)、左室后壁厚度(LVPWT)、左室舒张末期内径(LVEDd)、左室射血分数(LVEF),治疗后20周两治疗组重复测定上述指标。结果:与对照组相比常规治疗组和氯沙坦钾组P Ⅰ P、PⅢP、AngⅡ、醛固酮、LVEDd、LVMI水平明显升高(P<0.01),LVEF明显降低(P<0.01)。P Ⅰ P、PⅢP与LVEDd、LVMI呈正相关,与LVEF呈负相关(P<0.01)。经20周治疗后上述血检指标和超声心动图指标与治疗前比较在常规治疗组中无显著差异(P>0.05),在氯沙坦钾组血检指标和LVEDd、LVMI则显著降低(P<0.05),LVEF明显升高(P<0.05),治疗后的两组有显著差异(P<0.01)。结论:心衰患者心肌间质胶原增生致使心脏发生重构,氯沙坦钾有抑制心室重构作用。 Objective: To investigate the correlation of serum type I procollagen carboxy terminal pep-tide (P Ⅰ P)and type Ⅲ procollagen amino terminal peptide(P Ⅲ P) with heart failure and ventricular remodeling and the effects of losartan on that. Methods: 40 patients were divided randomly into conventional medication group, losartan group and 20 healthy cases belonged to control group. Serum concentrations of PⅠP, PⅢE P,angiotensin Ⅱ (Ang Ⅱ), aldosterone, interventricular septal thickness(IVST). left ventricular posterior wall thickness(LVPWT) , left ventricular end-diastolic diameter (LVEDd), left ventricular mass index(LV-MI) , left ventricular ejection fraction(LVEF) were respectively measured by radioimmunoassay and echocar-diogram in all the patients before and after 20 weeks treatment. Results:Serum level of P Ⅰ P,P Ⅲ P, Ang Ⅱ , aldosterone, IVST, LVEDd, LVMI were much higher and LVEF were much lower in two treatment guoups than in control group (P<0. 01). PIP, PEP, were correlated positively with LVEDd, LVMIL, and negatively with LVEF. PⅠP. P Ⅲ P, aldosterone , LVEDd, LVMI, were significantly lower and LVEF were much higher after medication than before medication. Conclusions: Collagen prolieration lead to left ventricular remodeling that deteriorates cardiac function, which can be inhibited by losartan.
出处 《国外医学(心血管疾病分册)》 2003年第5期310-312,共3页
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  • 1Goldstein S, Ali AS, Sabbah H, et al. Ventricular remodeling. Mechanism and prevention. Cardiol Clin, 1998,16(4):623-632.
  • 2Dzau VJ, Hirsch AT. Emerging role of tissue rennin-angiotensin systems in congestive heart failure. Eur Heart J, 1990,11 (Suppl B) :65-71.
  • 3Smits JF,van Krimpen C, Schoemaker RG, et al. Angiotensin Ⅱ receptor blockade after myocardial infarction in rats:effects on hemodynamics, myocardial DNA synthesis, and interstitial collagen content. J Cardiovasc Pharmacol, 1992,20(5) :772-778.
  • 4Taylor K, Patten RD, Smith JJ, et al. Divergent effects of angiotensin-converting enzyme inhibition and angiotensin Ⅱ receptor antagonism on myocardial cellular proliferation and collagen deposition after myocardial infarction in rats. J Cardiovasc pharmacol, 1998 ,31 (5) :654-660.
  • 5Jalowy A, Schulz R, Dorge H, et al. Infarct size reduction by ATI-receptor blockade through a signal cascade of AT2-receptor activation, bradykinin and prostaglandins in pigs. JAm Coil Cardiol, 1998 ,32(4): 1787-1796.
  • 6Goodfriend TL, Elliott ME, Catt KJ, et al. Angiotensin receptors and their antagonist. N Engl J Med, 1996,334(25),1649-1654.

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