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目的观察慢性容量超负荷在诱导大鼠心肌肥大模型中心肌组织中CT-1和Ang II含量的变化,进而探讨其可能机制。方法将SD大鼠随机分为正常组,伪手术组和容量负荷模型组,分别测量全心室重/体重比值、右心室重/体重比值和平均动脉压,检测血浆中肾素活性和Ang II含量,右心室的组织切片进行免疫组织化学检测。结果模型组与正常对照组及伪手术组比较心肌明显肥大且升高150%(P﹤0.01)。平均动脉压模型组或伪手术组与正常组比较差异均无统计学意义(P﹥0.05);血浆肾素活性模型组与伪手术组比降低(P﹤0.01),血浆Ang II含量模型组与伪手术组比升高(P﹤0.01);右心室CT-1免疫组化模型组与伪手术组的表达升高(P﹤0.05)。结论慢性容量超负荷可诱导大鼠心肌肥大,Ang II和CT-1可能是参与容量超负荷诱导心肌肥大反应的重要因素。
Objective To investigate the changes of CT-1 and Ang II contents in myocardial tissue induced by chronic volume overload in rat model of cardiac hypertrophy induced by ischemia, and to explore its possible mechanism. Methods The SD rats were randomly divided into normal group, sham operation group and volume load model group. The ratio of total body weight / body weight, right ventricular weight / body weight and mean arterial pressure were measured respectively. Plasma renin activity and Ang II content , Right ventricular tissue sections for immunohistochemistry. Results Compared with the normal control group and sham operation group, the myocardial hypertrophy in model group was significantly increased and increased by 150% (P <0.01). There was no significant difference between the mean arterial pressure model group and the sham operation group and the normal group (P> 0.05), the plasma renin activity model group was significantly lower than the sham operation group (P <0.01) (P <0.01). The expression of CT-1 in the right ventricle was higher than that in the sham operation group (P <0.05). Conclusion Chronic volume overload can induce cardiac hypertrophy in rats. Ang II and CT-1 may be involved in the capacity-overload induced cardiac hypertrophy.