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[氯沙坦、福辛普利对高血压大鼠心肌纤维化、血管紧张素II及心脏重塑的影响]

[Effects of lorsartan, fosinopril on myocardial fibrosis, angiotensin II and cardiac remolding in hypertensive rats].

作者信息

He B X, Yu G L, Liang X Q

机构信息

Department of Geriatric Cardiology, Xiangya Hospital, Central South University, Changsha 410008, China.

出版信息

Hunan Yi Ke Da Xue Xue Bao. 2001 Apr 28;26(2):118-20.

Abstract

OBJECTIVE

To investigate effects of lorsartan, fosinopril on myocardial fibrosis, angiotensin II and cardiac remolding in the spontaneously hypertensive rats (SHR).

METHODS

16-week-old SHRs were divided randomly into 3 groups: SHR-L (treated with lorsartan), SHR-F (treated with fosinopril) and SHR-C (untreated), each group consisting of 10 rats. After 8 weeks' and 16 weeks' therapeutic period, collagen volume fraction (CVF), perivascular circumferential area (PVCA), plasma and myocardium angiotensin II concentrations were examined by pathological examination with computed processing and radioimmunoassay respectively.

RESULTS

(1) Compared with SHR-C after 8 weeks' and 16 weeks' therapeutic period, the systolic blood pressure (SBP) was decreased similarly in both treatment groups. Heart and left ventricular weights, heart weight and eft ventricular mass indexes were lower significantly in both treatment groups than in SHR-C. Left ventricular mass index was reduced to a lower extent in SHR-F group than in SHR-L group after 16 weeks. (2) Compared with SHR-C, CVF, PVCA after 8 weeks and 16 weeks were reduced significantly in SHR-F and SHR-L. Meanwhile, CVF after 16 weeks in SHR-F than in SHR-L. (3) Compared with SHR-C after both therapeutic periods, plasma and myocardium angiotensin II concentrations were increased Significantly in SHR-L, but plasma angiotensin II concentrations were not altered significantly in SHR-F. However, myocardium angiotensin II concentrations were reduced significantly in SHR-F after 8 weeks and 16 weeks in SHR-F.

CONCLUSION

Lorsartan, fosinopril inhibit myocardial fibrosis and reverse heart hypertrophy. Fosinopril may be more effective in these above effects than Lorsartan. The mechanism of the both drug's cardioprotective effects was related to inhibition of myocardium rennin-angiotension-aldsteron system.

摘要

目的

探讨氯沙坦、福辛普利对自发性高血压大鼠(SHR)心肌纤维化、血管紧张素Ⅱ及心脏重塑的影响。

方法

将16周龄的SHR随机分为3组:SHR-L组(氯沙坦治疗组)、SHR-F组(福辛普利治疗组)和SHR-C组(未治疗组),每组10只大鼠。治疗8周和16周后,分别采用计算机处理病理检查和放射免疫法检测胶原容积分数(CVF)、血管周围圆周面积(PVCA)、血浆及心肌血管紧张素Ⅱ浓度。

结果

(1)治疗8周和16周后,与SHR-C组相比,两个治疗组的收缩压(SBP)均有相似程度的降低。两个治疗组的心脏和左心室重量、心脏重量及左心室质量指数均显著低于SHR-C组。16周后,SHR-F组的左心室质量指数降低程度低于SHR-L组。(2)与SHR-C组相比,SHR-F组和SHR-L组在8周和16周时的CVF、PVCA均显著降低。同时,SHR-F组16周时的CVF低于SHR-L组。(3)两个治疗期后,与SHR-C组相比,SHR-L组的血浆及心肌血管紧张素Ⅱ浓度显著升高,但SHR-F组的血浆血管紧张素Ⅱ浓度无显著变化。然而,SHR-F组在8周和16周时心肌血管紧张素Ⅱ浓度显著降低。

结论

氯沙坦、福辛普利可抑制心肌纤维化并逆转心脏肥大。福辛普利在上述作用方面可能比氯沙坦更有效。两种药物心脏保护作用的机制均与抑制心肌肾素-血管紧张素-醛固酮系统有关。

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