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目的 :观察卡托普利对压力负荷性心肌肥厚大鼠心肌组织中的血管紧张素 (MAng )及一氧化氮合成酶 (NOS)含量的影响。方法 :本实验采用腹主动脉缩窄法建立大鼠压力负荷性心肌肥厚模型 ,用放免法测定 MAng 及比色法测定 NOS含量。结果 :腹主动脉缩窄后 4周 ,心脏重量与 MAng 含量显著增加 ,NOS也代偿性增加 ,而血浆 Ang (PAng )变化不明显 ;卡托普利能降低全心重 /体重比值 ,增加 NOS活性 ,降低MAng 含量。结论心脏肾素 -血管紧张素系统 (RAS)与NO/NOS系统参与了心肌肥厚的发生发展 ,卡托普利通过作用上述环节逆转心肌肥厚
Objective: To observe the effects of captopril on the content of angiotensin (MAng) and nitric oxide synthase (NOS) in myocardium of pressure-overload hypertrophic rats. Methods: The rat model of pressure-overload cardiac hypertrophy was established by abdominal aorta constriction. The content of NOS was determined by radioimmunoassay (MAng) and colorimetry. Results: 4 weeks after abdominal aorta constriction, heart weight and MAng content increased significantly, NOS also compensatory increase, but plasma Ang (PAng) did not change significantly; captopril can reduce the whole heart weight / body weight ratio, increased NOS activity, reduce MAng content. Conclusions Cardiac renin-angiotensin system (RAS) and NO / NOS are involved in the development of cardiac hypertrophy. Captopril reversed the effects of cardiac hypertrophy