血压平逆转肾性高血压大鼠左室重构的作用及机制

目的　探讨复方中药制剂血压平逆转二肾一夹 (2K1C)肾性高血压大鼠左室重构的作用及机制。方法　采用 2K1C法 ,建立肾性高血压大鼠 (RHR)模型 ,术后 8周将造模成功的 40只RHR随机分为 5组 ,每组 8只 ,采用放免法检测血清Ⅲ型前胶原(PCⅢ ) ,测量心肌细胞面积、周长、平均直径、长径和短径。SP免疫组化测量原癌基因C -myc和C -fos表达阳性细胞的平均光密度值。结果　①血压平有降低血压、左室重量 (LVW )、左室重量指数 (LVW /BW )、心肌细胞体积的作用 ;②血压平可降低血清PCⅢ含量 ,抑制原癌基因C -myc和C -fos的表达 ;③血压平的降压和逆转左室重构的药理作用有量效关系。结论　血压平具有逆转RHR左室重构的作用 ,其降低血压、降低血清PCⅢ含量、抑制Ⅲ型胶原合成、防治心肌纤维化及降低原癌基因C -myc和C -fos的表达、抑制心肌细胞肥大、减轻左心室肥厚 ,是其逆转2K1CRHR左室重构的部分机制。

Effect and Mechanism of Xueuyaping on Left Ventricle Remodeling in Renal Hypertension

Objective To explore the reverse effect and its mechanism of Xueyaping on left ventricle remodeling resulting from renal hypertension induced by 2K1C in rats.Methods Renal hypertension rat(RHR) was induced by 2K1C. 40 RHRs were divided into 5 groups randomly with 8 rats in each group.The left ventricle and interventricular septal weight (LVW) were measured. LVW/BW ratio were calculated. Serum PCIII was measured using radio-immune methods. Paraffin embedded heart tissue was cut and stained with HE. Area, circle length, mean diameter, length of long and short axes of heart muscle cells were measured using high resolution picture analyzing system. Paraffin embedded heart tissue was also stained with SP immuno-histochemistry. Mean light density of positive C-myc and C-fos expression cell were measured using high resolution analyzing system.Results 1. Xueyaping had the effect of lowering blood pressure, decreasing LVW, LVW/BW and heart muscle cell volume. SBP, LVW and LVW/BW.2.Xueyaping could decrease serum PCIII, decrease the expression of C-myc and C-fos.3. Blood lowering and remodeling reversing effects of Xueyaping had a dosage-effect relationship.Conclusion Xueyaping has the effects of reversing left ventricle remodeling in hypertensive rats induced 2K1C. Its effects of lowering blood, lowering serum PCIII decreasing the synthesis of type III collagen, preventing fibrosis of heart muscle and decreasing the expression of C-myc and C-fos,depressing the hypertrophy of myocyte, decreasing left ventricle hypertrophy, etc, might be the partial mechanism of reversing left ventricle remodeling in hypertensive rats induced by 2K1C.