中华医学杂志（英文版）2002，Vol.115Issue(3)：364-366,3.
缬沙坦对自发性高血压大鼠心肌细胞凋亡的影响
Influence of Valsartan on myocardial apoptosis in spontaneously hypertensive rats
李为民 1孙宁玲 2刘巍 1陈源源 2虞有智2
作者信息
- 1. 哈尔滨医科大学第一临床医学院心内科,哈尔滨,150001
- 2. 北京医科大学人民医院心内科,北京,100044
- 折叠
摘要
Abstract
Objective To explore the pathogenic changes of myocardial apoptosis in heart hypertrophy during hypertension and evaluate the anti-apoptosis effect of Valsartan. Methods Thirty spontaneously hypertensive rats (SHRs) were divided into two groups: 15 treated with Valsartan (20?mg*kg-1*d-1) (SHR+Valsartan group), the others with placebo (SHR+placebo group), with 15 normal Wistar rats as control. Systolic blood pressure was measured by the tail-cuff method. The observation period was from 8 to 16 weeks of age. Cardiac apoptosis was evaluated by a Terminal Deoxynucleotidyl Transferase-Mediated dUTP-biotin Nick End Labeling (TUNEL) assay. Results Mean blood pressure values were 127±2?mm?Hg in controls, 163±6?mm?Hg in the SHR+Valsartan group and 193±7?mm?Hg in the SHR+placebo group at 16 weeks of age, whereas the blood pressure in 8-week-old SHR and Wistar rats were 175±3?mm?Hg and 125±5?mm?Hg, respectively. The ratio of the heart weight over body weight declined in Wistar (3.07±0.03?mg/g) and SHR+Valsartan groups (3.22±0.19?mg/g) compared with the SHR+placebo group (4.02±0.31?mg/g) (P<0.05). The density of TUNEL-positive cells in Wistar and SHR±Valsartan groups was 23.3±3.3 nuclei/HPF and 35.0±1.3 nuclei/HPF, both of which were significantly less than that of the SHR+placebo group (116.7±11.3 nuclei/HPF). Conclusions In response to chronic pressure overload, cardiomyocyte-specific apoptosis contributes to the transition from compensatory hypertrophy to decompensation. Apoptosis may be effectively inhibited by Valsartan in the early stage of hypertension. 关键词
心肌肥厚 心力衰竭 细胞凋亡 TUNEL 缬沙坦Key words
cardiac hypertrophy/heart failure/apoptosis/TUNEL/Valsartan分类
医药卫生引用本文复制引用
李为民,孙宁玲,刘巍,陈源源,虞有智..缬沙坦对自发性高血压大鼠心肌细胞凋亡的影响[J].中华医学杂志（英文版）,2002,115(3):364-366,3.
