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目的研究长期被动跑轮运动诱导的大鼠心肌肥厚,探索新的生理性心肌肥厚动物模型。方法雄性8周龄SPF级SD大鼠40只随机分为正常对照组、被动跑轮运动组、假手术组和主动脉弓缩窄组,各10只。对被动跑轮运动组和主动脉弓缩窄组大鼠分别行被动跑轮运动训练和主动脉弓缩窄术;正常对照组不作任何处理;假手术组不结扎胸主动脉,其他与主动脉弓缩窄组作相同处理。训练或术后5周,被动跑轮运动和主动脉弓缩窄两组模型分别与正常对照组和假手术组进行比较,从超声心动图、组织形态学、心衰分子标记物表达等方面来全面评估被动跑轮运动建立生理性心肌肥厚的效果。结果超声心动图结果显示,被动跑轮运动组和主动脉弓缩窄组的左室前壁厚度均较各自对照组明显增加(P<0.01);在每搏输出量和射血分数方面,被动跑轮运动组和主动脉弓缩窄组与各自的对照组比较,亦均有明显变化(P<0.01)。被动跑轮运动组的左心室舒张末期内径较正常对照组无明显改变,而主动脉弓缩窄组较假手术组减少38%(P<0.01),提示两种不同的心脏肥厚导致的心脏结构改变有明显差别。组织形态学方面,较正常对照组,被动跑轮运动组心脏质量指数增加25.0%,左室质量指数增加37.3%,肺脏质量指数增加23.8%;与假手术组比较,主动脉弓缩窄组的上述指标分别增加31.6%、38.8%和56.6%(P<0.05或P<0.01)。被动跑轮运动组心房利钠肽(ANP)和脑钠肽(BNP)的蛋白表达量明显降低,分别为正常对照组的0.67倍和0.48倍(P<0.05);而主动脉弓缩窄组ANP、BNP较假手术组分别升高1.98倍和2.03倍,差异有统计学意义(P<0.05)。结论长期被动跑轮运动能成功诱导大鼠生理性心肌肥厚,为建立生理性心肌肥厚的动物模型提供了新的方法。
Objective To investigate the cardiac hypertrophy in rats induced by long-term passive runner exercise and to explore a new animal model of physiological cardiac hypertrophy. Methods Forty male Sprague-Dawley (SD) SD rats aged 8 weeks were randomly divided into normal control group, passive exercise group, sham operation group and aortic arch constriction group. Passive runner exercise training and aortic arch aortic arch were performed on passive runner group and aortic arch constriction group respectively; no treatment was given in normal control group; sham operation group was not ligation of thoracic aorta, others were the same as aortic arch constriction group deal with. Two weeks after training or 5 weeks after operation, passive run-length motion and aortic arch constriction were compared with those in normal control group and sham-operated group, respectively. Echocardiography, histomorphology and molecular marker of heart failure were all evaluated Passive runner exercise to establish the effect of physiological myocardial hypertrophy. Results The results of echocardiography showed that the anterior wall thickness of the left ventricle of passive runner group and aortic arch constriction group was significantly higher than that of the control group (P <0.01). In stroke volume and ejection fraction, passive runner Exercise group and aortic arch constriction group compared with the respective control group, also had significant changes (P <0.01). The left ventricular end-diastolic diameter of the passive runner group was significantly lower than that of the normal control group, while the aortic arch narrowing group was 38% less than that of the sham-operated group (P <0.01), suggesting that the cardiac structural changes caused by two different types of cardiac hypertrophy were Obvious difference. Histomorphology, compared with the normal control group, the heart rate index of passive runner group increased 25.0%, the left ventricular mass index increased 37.3% and the lung mass index increased 23.8%. Compared with the sham operation group, the above indexes of aortic arch narrowing group Increased by 31.6%, 38.8% and 56.6% respectively (P <0.05 or P <0.01). The protein expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in passive runner group decreased significantly, which were 0.67 and 0.48 times higher than those in normal control group (P <0.05) Compared with sham operation group, BNP increased 1.98 times and 2.03 times respectively, the difference was statistically significant (P <0.05). Conclusion Long-term passive runner exercise can induce physiological cardiac hypertrophy in rats, which provides a new method for establishing an animal model of physiological cardiac hypertrophy.