论文部分内容阅读
目的:探讨抗纤益心方抑制扩张型心肌病(DCM)大鼠血浆血管紧张素Ⅱ和醛固酮的机制。方法:采用自主饮用呋喃唑酮水溶液(按1 kg水加700 mg呋喃唑酮配置)建立DCM大鼠模型,分为模型组、抗纤益心方高、低剂量组、卡托普利对照组、中西药联用组。每日分别给予生理盐水,抗纤益心方18.8,4.7 g·kg-1,卡托普利10.125 mg·kg-1,抗纤益心方高剂量和卡托普利混合溶液,ig干预8周,用放射免疫法检测血浆血管紧张素Ⅱ和醛固酮含量。结果:模型组大鼠血浆中血管紧张素Ⅱ(159.94±12.03)ng·L-1和醛固酮(1.23±0.09)μg·L-1明显高于正常组(69.47±7.79)ng·L-1和(0.34±0.11)μg·L-1(P<0.05);与模型组比较,所有给药组(抗纤益心方小剂量组除外)血浆中血管紧张素Ⅱ和醛固酮明显下降(P<0.05);抗纤益心方18.8 g·kg-1组与卡托普利10.125 mg·kg-1组相比无显著差异,血管紧张素Ⅱ分别为(85.23±5.18),(87.90±6.02)ng·L-1,醛固酮分别为(0.69±0.06),(0.74±0.42)μg·L-1(P>0.05),与中西药联用组比较有统计学意义(P<0.05),与小剂量组比较有显著差异(P<0.05)。结论:抗纤益心方能够干预扩张型心肌病大鼠左室重构,其作用可能与抑制血浆中血管紧张素Ⅱ及醛固酮的水平有关。
Objective: To investigate the mechanism of Kangxixiyixin Fang inhibiting plasma angiotensin Ⅱ and aldosterone in dilated cardiomyopathy (DCM) rats. Methods: A rat model of DCM was established by self-administered furazolidone solution (1 kg water plus 700 mg furazolidone). The rats were divided into model group, high and low anti-fibrosis group, captopril control group, Use group. The rats were given daily saline, anti-fibrosis 18.8,4.7 g · kg-1, captopril 10.125 mg · kg-1, anti-fibrosis and high-dose side captopril mixed solution, ig intervention 8 Weeks, plasma radioimmunoassay angiotensin Ⅱ and aldosterone levels. Results: The plasma levels of angiotensin Ⅱ (159.94 ± 12.03) ng · L-1 and aldosterone (1.23 ± 0.09) μg · L-1 in model group were significantly higher than those in normal group (69.47 ± 7.79 ng · L-1) (0.34 ± 0.11) μg · L -1 (P <0.05). Compared with the model group, the plasma levels of angiotensin Ⅱ and aldosterone in all the groups except Kangxian Yixin Fang low-dose group were significantly decreased (P <0.05 ). There was no significant difference between the anti-fibrosis prescription 18.8 g · kg-1 group and the captopril 10.125 mg · kg-1 group (85.23 ± 5.18), (87.90 ± 6.02) ng The levels of L-1 and aldosterone were (0.69 ± 0.06) and (0.74 ± 0.42) μg · L-1, respectively (P> 0.05) There was significant difference between the two groups (P <0.05). Conclusion: Kangxian Yixin Recipe can interfere with left ventricular remodeling in rats with dilated cardiomyopathy, which may be related to the inhibition of plasma levels of angiotensin Ⅱ and aldosterone.