liguzinediol对压力超负荷大鼠心室重构的影响

目的通过部分结扎大鼠肾上腹主动脉建立压力超负荷性心室肥厚模型,观察liguzinediol对各组大鼠心室重构的影响。方法用腹主动脉缩窄方法复制大鼠压力超负荷心室重构模型。设假手术组,模型组,liguzinediol高、中、低剂量(20、10、5 mg.kg-1)组及阳性药(卡托普利10 mg.kg-1)组。造模后稳定1周开始灌胃给药,给药8周后测量大鼠心脏动脉收缩压(SBP)、动脉舒张压(DBP)、平均动脉压(MAP)、左室收缩内压(LVSP)、左室舒张末期压(LV-EDP)、左心室内压最大上升/下降速率(±dp/dtmax);计算全心质量指数(HMI)以及左室质量指数(LVMI);HE染色光镜观察心肌结构;放射免疫法检测大鼠血浆中肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD);碱水解法测羟脯氨酸(HYP)含量,ELISA法检测大鼠心肌组织Ⅰ/Ⅲ型胶原比值。结果 liguzinediol能明显降低压力超负荷致心室重构大鼠的HMI和LVMI,改善血流动力学参数,降低AngⅡ和ALD含量,降低HYP含量及Ⅰ/Ⅲ型胶原比值。结论 liguzinediol具有抑制实验性心室重构的作用,其机制与抑制心肌肾素-血管紧张素-醛固酮系统(RAAS)活性有关。

hmbian@sina.com Effect of liguzinediol on ventricular remodeling in press-overloaded rats

Aim To examine the effect of liguzinediol on ventricular remodeling induced by pressure overload in rats,as well as to explore the mechanisms involved.Methods The model rats in which ventricular remodeling was induced with abdominal aortic banding(AAB) were randomly divided into 6 groups: Sham group,AAB model group,AAB plus captopril group(10 mg·kg-1),AAB plus liguzinediol groups with various dosages(5,10 and 20 mg·kg-1).After administration of the tested drugs for 8 weeks,SBP,DBP,MAP,LVSP,LVEDP and ±dp/dtmax were recorded.Heart mass index(HMI) and left ventricular mass index(LVMI) were calculated.Isolated rat hearts were observed by hematoxylin-eosin(HE) staining.The concentrations of renin,angiotensinⅡ(AngⅡ) and aldosterone(ALD) in plasma were measured by radioimmunoassay.The content of myocardial tissue hydroxyproline(HYP) was detected by alkaline hydrolysis,and the ratio of Ⅰ/Ⅲ type collagen was exam-ined by ELISA.Results Compared with model group, liguzinediol groups could significantly decrease hemodynamic parameters,HMI and LVMI,improve pathological changes,reduce AngⅡand ALD content in left ventricular tissue,decrease HYP content and the ratio of Ⅰ / Ⅲ type collagen.Conclusion In conclusion,liguzinediol significantly attenuates ventricular remodeling induced by pressure overload in rats.The benefi-cial mechanisms are in part associated with its alleviating the activation of renin-angiotensin-aldosterone system.