摘要目的探讨遗传性高血压及心肌肥厚过程中心肌细胞凋亡的意义及AT1受体拮抗剂缬沙坦对其的影响. 方法　实验动物为8周龄自发性高血压大鼠（SHR）,分为缬沙坦治疗组（SHR+缬沙坦组）和非治疗组（SHR无药组）,以Wistar鼠作为正常血压对照,观察期限为8-16周.采用TUNEL染色法检测心肌组织凋亡细胞数. 结果　缬沙坦治疗后血压降至163±6?mm?Hg,与治疗前175±3?mm?Hg及无药组193±7?mm?Hg比较显著降低.SHR+缬沙坦组心脏指数3.22±0.19?mg/g,较SHR无药组4.02±0.31?mg/g显著降低.SHR+缬沙坦组与SHR无药组比较,前者TUNEL阳性细胞数显著减少至接近Wistar组. 结论　心肌细胞凋亡是代偿性心肌肥厚发展为心力衰竭的可能机制之一.高血压病早期缬沙坦在降压同时有效抑制心肌细胞凋亡.

abstractsObjective 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.