目的 研究葛根素對舒張性心力衰竭（distolic heart failure，DHF）大鼠心肌僵硬度和心肌組織Ⅰ型、Ⅲ型膠原表達(dá)的影響。方法 Wistar大鼠腹主動脈縮窄法建立DHF模型，術(shù)后4周，隨機分為4組（n=10），模型組，葛根素高、中、低劑量組（180、120、80 mg/kg），另有假手術(shù)組10只。連續(xù)給予相應(yīng)處理4周后，通過十六導(dǎo)生理記錄儀測量所得的血流動力學(xué)指標(biāo)計算大鼠心肌僵硬度常數(shù)（K），并應(yīng)用免疫組化法測定心肌組織Ⅰ、Ⅲ型膠原的表達(dá)。結(jié)果 與模型組比較，葛根素高劑量組K值無變化（P＞0.05），中劑量組K值顯著低于模型組（P＜0.01），低劑量組K值明顯低于模型組（P＜0.05）。與模型組比較，葛根素高劑量組心肌I型膠原蛋白表達(dá)明顯減弱（P＜0.05），心肌Ⅲ型膠原表達(dá)明顯增強（P＜0.05）；中劑量組心肌I型膠原蛋白表達(dá)顯著減弱（P＜0.01），心?、笮湍z原蛋白表達(dá)顯著增強（P＜0.01）；低劑量組心肌I型膠原蛋白表達(dá)明顯減弱（P＜0.05），心肌Ⅲ型膠原表達(dá)明顯增強（P＜0.05）。結(jié)論 葛根素中、低劑量能夠降低DHF大鼠心肌僵硬度，其作用機制與心?、裥湍z原、Ⅲ型膠原的表達(dá)有關(guān)。

Objective To study the effects of different doses of puerarin on stiffness in myocardium and expression of collagen type I and Ⅲ in diastole heart failure (DHF) rat models. Method DHF models were established by narrowing abdominal aorta in wistar rats. Four weeks after operation, DHF rats were divided into four groups randomly as follows, model group, puerarin high-, mid-, and low-dose groups (180, 120, 80 mg/kg), and sham operation group (n=10). After four-week administration, the stiffness of rat cardiac (K) was calculated by hemodynamics which measured by 16 physiologic recorder. The expression of collagen type I and Ⅲ was examined by immunohistochemical method. Results Compared with model group, K of the puerarin high-dose group did not change (P>0.05), K of the mid-dose group was significantly lower (P<0.01), K of the low-dose group was significantly lower (P<0.05). Compared with model group, the expression of collagen type I was significantly decreased (P<0.05), type Ⅲ was significantly enhanced (P<0.05) in puerarin high-dose group. The expression of collagen type I was significantly decreased (P<0.01), type Ⅲ was significantly enhanced (P<0.01) in puerarin mid-dose group. The expression of collagen typeⅠwas decreased significantly (P<0.05), type Ⅲ was significantly enhanced (P<0.05) in puerarin low-dose group. Conclusion Puerarin of middle and low doses could improve myocardial stiffness of DHF rats, and its mechanism is related with the expression of collagen type I and Ⅲ.