Suppr超能文献

氯沙坦、福辛普利与氨氯地平对高血压大鼠心肌细胞凋亡及左心室重构的对比研究

[Contrast of losartan, fosinopril and amlodipine on cardiomyocyte apoptosis and left ventricular remolding in hypertensive rats].

作者信息

Yu G L, Liang X Q, Zheng J 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 Oct 28;26(5):405-8.

Abstract

OBJECTIVE

To investigate effects of losartan, fosinopril and amlodipine on cardiomyocyte apoptosis, cardiac remolding in the spontaneously hypertensive rats (SHR).

METHODS

SHRs were treated with lorsartan (SHR-L), fosinopril (SHR-F), amlodipine (SHR-A), and untreated (SHR-C) respectively for 8 and 16 weeks. Cardiomyocyte apoptotic index (APOI), left ventricular mass, left ventricular mass index (LVM, LVMI), and plasma and myocardium angiotensin II(PAng II, MAng II) concentrations were examined.

RESULTS

  1. The systolic blood pressure was decreased similarly in all treatment groups in 8 and 16 weeks. LVMIs were reduced significantly in all treatment groups. LVMI was significantly lower in SHR-F group than that in other two treatment groups in 16 weeks. 2. APOIs were decreased significantly in SHR-F group in 8 weeks and in all treatment groups, especially in SHR-F group in 16 weeks. 3. Compared with SHR-C group in both periods, PAng II and MAng II were significantly increased in SHR-L group, but MAng II concentration was only decreased significantly in SHR-F group in 8 weeks, and in SHR-F and SHR-A groups in 16 weeks.

CONCLUSION

Losartan, amlodipine, and especially fosinopril can inhibit cardiomyocyte apoptosis, prevent myocardial fibrosis, and reverse heart hypertrophy. Inhibition of myocardium rennin--angiotension--aldsteron system may be the mechanism of the three drugs' cardioprotective effects.

摘要

目的

探讨氯沙坦、福辛普利和氨氯地平对自发性高血压大鼠(SHR)心肌细胞凋亡及心脏重塑的影响。

方法

将SHR分别用氯沙坦(SHR-L)、福辛普利(SHR-F)、氨氯地平(SHR-A)治疗,未治疗组(SHR-C)作为对照,疗程均为8周和16周。检测心肌细胞凋亡指数(APOI)、左心室质量、左心室质量指数(LVM、LVMI)以及血浆和心肌组织血管紧张素II(PAng II、MAng II)浓度。

结果

  1. 所有治疗组在8周和16周时收缩压均有相似程度下降。所有治疗组的LVMI均显著降低。16周时,SHR-F组的LVMI显著低于其他两个治疗组。2. 8周时SHR-F组的APOI显著降低,16周时所有治疗组的APOI均显著降低,尤其是SHR-F组。3. 与两个时期的SHR-C组相比,SHR-L组的PAng II和MAng II显著升高,但仅8周时SHR-F组的MAng II浓度显著降低,16周时SHR-F组和SHR-A组的MAng II浓度显著降低。

结论

氯沙坦、氨氯地平,尤其是福辛普利可抑制心肌细胞凋亡,预防心肌纤维化,逆转心脏肥大。抑制心肌肾素-血管紧张素-醛固酮系统可能是这三种药物心脏保护作用的机制。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验