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目的观察阿折地平对自发性高血压大鼠(spontaneous hypertension rat,SHR)心肌肥厚的抑制作用,初步探讨阿折地平抑制和逆转左心室肥厚(left ventricular hypertrophy,LVH)的可能机制。方法 20只SHR随机分为阿折地平组和SHR组,另选同源同系、血压正常的Wistar-Kyoto大鼠10只作为正常对照组(WKY组),分别给予阿折地平(3mg.kg-1)和生理盐水灌胃,所有大鼠10周后测定收缩压(SBP)、心率(HR)、左心室重量指数(LVW/BW)、血清和心肌组织中一氧化氮(NO)和肿瘤坏死因子(TNF-α)含量。结果 SHR组与WKY组比较,SHR组SBP、LVW/BW明显升高(P<0.05),血清和心肌中NO含量明显降低(P<0.05),TNF-α含量明显升高(P<0.05);应用阿折地平治疗10周后,SHR组与阿折地平组比较,阿折地平组SBP、LVW/BW有所升高(P<0.05),血清和心肌中NO含量明显升高(P<0.05),TNF-α含量明显降低(P<0.05)。结论阿折地平可以抑制高血压大鼠心肌肥厚,机制可能与其升高NO水平,抑制TNF-α表达有关。
Objective To observe the inhibitory effect of aztrendin on cardiac hypertrophy in spontaneous hypertensive rats (SHR) and to explore the possible mechanism of the adverse effects of aztrendipine and reverse left ventricular hypertrophy (LVH). Methods Twenty SHRs were randomly divided into two groups: the atazapine group and the SHR group. Ten Wistar-Kyoto rats with the same blood pressure were selected as normal control group (WKY group) (SBP), heart rate (HR), left ventricular mass index (LVW / BW), serum and myocardial nitric oxide (NO) and tumor necrosis Factor (TNF-α) content. Results Compared with WKY group, the SBP and LVW / BW in SHR group were significantly increased (P <0.05), while the levels of NO in serum and myocardium were significantly decreased (P <0.05) and TNF- Compared with the patients in the azodem group, the levels of SBP and LVW / BW increased in the SHR group (P <0.05) and the content of NO in the serum and myocardium increased significantly (P < 0.05). The content of TNF-α decreased significantly (P <0.05). Conclusion Aztrendipine can inhibit cardiac hypertrophy in hypertensive rats, which may be related to the increase of NO level and the inhibition of TNF-α expression.