压力负荷增加大鼠心肌和血浆血管紧张素Ⅱ的改变及鹿角方的作用

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观察压力负荷增加大鼠心肌组织和血浆血管紧张素Ⅱ(AugⅡ)的改变及鹿角方的作用。方法:采用实验性腹主动脉狭窄所致压力负荷增加大鼠充血性心力衰竭心肌肥厚模型,观察左室质量指数(LVMI);采用放射免疫法检测心肌组织和血浆Ang Ⅱ水平。结果:LVMI模型组明显高于假手术组(P<0.001),鹿角方大、小剂量组与模型组比较均有明显下降(P<0.01, P<0.05);左室心肌Ang Ⅱ水平模型组较假手术组显著升高(P<0.001),鹿角方大、小剂量组与模型组比较均有明显下降(P<0.001);血浆AngⅡ水平模型组较假手术组显著升高(P<0.001),鹿角方大、小剂量组与模型组比较均有明显下降(P<0.01)。结论:压力负荷增加使充血性心力衰竭心肌肥厚大鼠心肌组织和血浆血管 Ang Ⅱ水平明显升高;鹿角方可显著降低大鼠心肌组织和血浆Ang Ⅱ水平;鹿角方治疗充血性心力衰竭的疗效,可能与该方降低心肌和血浆Ang Ⅱ水平、逆转左室肥厚的作用有关。 Observed the increase of pressure load in rats myocardial tissue and plasma angiotensin II (Aug II) changes and the role of antler square. Methods: The experimental model of myocardial hypertrophy in congestive heart failure was induced by pressure overload induced by abdominal aortic stenosis. Left ventricular mass index (LVMI) was observed. Ang II levels in myocardial tissue and plasma were detected by radioimmunoassay. RESULTS: The LVMI model group was significantly higher than the sham operation group (P<0.001). Compared with the model group, the antlerfang large and small dose groups were significantly decreased (P<0.01, P<0.05); The level of myocardial Ang II in the model group was significantly higher than that in the sham operation group (P<0.001). Both the large and small doses of antlerfang and the model group were significantly decreased compared with the model group (P<0.001); plasma Ang II levels in the model group were lower than those in the model group. The sham operation group was significantly increased (P<0.001), and the antler square large and small dose groups were significantly decreased compared with the model group (P<0.01). Conclusion: The increase of pressure load increases the level of Ang II in myocardium and plasma of rats with congestive heart failure and myocardial hypertrophy. The antler prescription can significantly reduce the level of Ang II in myocardial tissue and plasma in rats. The curative effect of Lujia recipe in the treatment of congestive heart failure. , May be related to the side to reduce myocardial and plasma Ang II levels, the role of reversal of left ventricular hypertrophy.
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