摘要
目的以原发性高血压大鼠(SHR)为实验模型,观察单纯使用血脂康对SHR血压、左室功能的影响,并探讨其相关机制。方法10周龄雄性SHR和WKY按试验和对照的原则分为三组:正常对照组(WKY),实验对照组(SHR),血脂康组(SHR-X,SHR服血脂康2400mg.kg-1.d-1),饲养16周后观察鼠尾收缩压(SBP),有创心功能,左心室心肌肥厚指数(LVM I),血浆内皮素-1(ET-1),肌浆网Ca2+-ATP酶活性(SERCA)。心肌细胞横径(TDM),心肌胶原含量及分布情况。结果SHR-X组较SHR组SBP低17.02mm Hg;左心室等容舒张期室内压下降的时间常数(T)显著降低[(1.01±0.09)m s,(2.38±0.59)m s,P<0.05];LVM I有明显下降[(3.07±0.25)mg/g,(3.31±0.23)mg/g,P<0.05]。ET-1有明显降低[(138±26pg/m l,(197±39)pg/m l,P<0.01),SERCA活性稍有升高。结论血脂康对延缓SHR血压的上升产生一定影响,有助于改善SHR左心室舒张功能,有助于抑制SHR左室肥厚。血脂康对心脏重构逆转的作用机制可能涉及血清ET-1水平下降,提高心肌细胞SERCA活性,抑制SHR心肌细胞内[Ca2+]i超载等环节。
Objective To observe the effects of xuezhikang ventricular function and the change of left ventricular hypertrophy investigate the mechanism of this functional changes. Methods therapy on systolic blood pressure(SBP),left in spontaneously hypertensive rats(SHR). To The male SHRs and WKYs which were 10 - week old were divided into 3 groups by feeding with different medicines:the normal control group( WKY group, n =9),experimental control group( SHR group, n = 10) and SHR- X group( SHR treated with xuezhikang 2400mg· kg^-1· d^-1 ,n = 11 ). The rats were studied the tail- cuff systolic blood pressure(SBP) ,invasive left ventricular function, left ventricle mass index( LVMI), serum level of endothelin -1 (ET -1 )and the activity of sarcoplasmic reticulum Ca^2+ - ATPase(SERCA) in left ventricle after therapy for 16 weeks. Results Compared with SHR group :SBP showed 17.02mmHg lower in SHR -X . Time constant was significant lower in SHR -X [(1.01±0.09)ms vs(2.38 ±0.59)ms, P 〈0.05] ,left ventricle mass index(LVMI) was lower in SHR -X [ (3.07±0.25 ) mg/g vs (3.31 ± 0.23) mg/g, P 〈 0.05 ]. Serum level of ET - 1 was significant lower in SHR -X [ (138± 26)pg/ml vs (197±39)pg/ml, P 〈0.01 ]. The activity of SERCA in left ventricle was a little higher in SHR - X. Conclusion The therapy of xuezhikang might have some effects to delay blood pressure increasing in SHR. Xuezhikang could improve left ventricular diastolic function. Xuezhikang could effectively inhibit left ventrical hypertrophy. The mechanisms of these effects might involve the amelioration of blood vessel endothelium function,reduction of the serum level of ET- 1 and increase the activity of SERCA to inhibit cardiac myocyte [ Ca^2+] i overload.
出处
《中原医刊》
2006年第14期5-8,共4页
Central Plains Medical Journal
基金
广东省2005年自然科学基金项目课题(5002313)
关键词
血脂康
高血压
左心室功能
心脏重构
Xuezhikang
Hypertension
Left ventricular function
Cardiac remodeling