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蔡辉,胡婉英,董耀荣,赵卫.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[J].中国中西医结合杂志,2000,(4):282-283,285
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
Changes of Myocardial Tissue and Plasma Angiotensin Ⅱ in Rats with Pressure Overload and Effect of Lujiao Prescription
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DOI:
中文关键词:  充血性心力衰竭  心肌肥厚  压力负荷  血管紧张素Ⅱ  鹿角方
英文关键词:congestive heart failure  myocardial hypertrophy  pressure overload  angiotensin Ⅱ  Lujiao prescription
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作者单位
蔡辉 CAI Hui, HU Wanying, DONG Yaorong, et al (Naming General Hospital of Naming Military Area, Nanjing (210002 
胡婉英 CAI Hui, HU Wanying, DONG Yaorong, et al (Naming General Hospital of Naming Military Area, Nanjing (210002 
董耀荣 CAI Hui, HU Wanying, DONG Yaorong, et al (Naming General Hospital of Naming Military Area, Nanjing (210002 
赵卫 CAI Hui, HU Wanying, DONG Yaorong, et al (Naming General Hospital of Naming Military Area, Nanjing (210002 
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中文摘要:
      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。
英文摘要:
      To observe the changes of myocardial tissue and plasma angiotensin Ⅱ in rats with pressure overload and effect of Lujiao prescription (LJP). Methods: Left ventriculagr mass index (LVMI), cardiac tissue and plasma angiotensin Ⅱ were measured in the rat model with myocardial hypertrophy of congestive heart failure and pressure overload by abdominal aortic constriction by radioimmunoassay. Results: LVMI level in the model group was obviously higher than that of the sham group (P<0.001), while in LJP groups (both groups of low and high dose) was lowered significantly as compared with the model group. The myocardial and plasma angiotensin Ⅱ levels in the model group were obviously higher than those of the sham group (P<0.001), while those of the LJP groups were also lowered significantly (P<0.001). Conclusions: Cardial tissue and plasma angiotensin Ⅱ in rats with myocardial hypertrophy of congestive heart failure by pressure overload were Increased, and LJP could decrease them significantly. The therapeutic mechanism of LJP in treating heart failure might be related with the lowering of angiotensin Ⅱ in cardial tissue and plasma so as to reduce the left ventricular hypertrophy.
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