中文摘要：

目的探讨SO2吸入对运动大鼠心肌胶原纤维形态及胶原蛋白含量的影响。方法24只雄性SD大鼠随机分为空白对照组、单纯运动组、单纯SO2污染组、SO2污染运动组，每组6只。单纯运动组、空白对照组大鼠置于自然环境中，单纯SO2污染组、SO2污染＋运动组置于人工模拟的SO2污染环境中（10mg／m2，1h／d，连续4周），单纯运动组、SO2污染＋运动组大鼠进行跑轮运动（8ndmin，1h／d，连续4周）。采用胃酶酸解法测定大鼠心肌羟脯氨酸的含量，并计算胶原浓度。采用苦味酸一天狼猩红染色法检测大鼠心肌、小动脉周围胶原容积分数。结果单纯运动组、单纯SO2污染组和SO2污染＋运动组大鼠心肌胶原纤维较空白对照组增生，且SO2污染＋运动组大鼠心肌胶原纤维过度堆积。SO2污染＋运动组、单纯SO2污染组、单纯运动组大鼠心肌羟脯氨酸含量、胶原浓度较空白对照组升高（P〈0．05），SO2污染＋运动组升高更明显（P〈0．01）；单纯SO2污染组、SO2污染＋运动组心肌、小动脉血管周围胶原容积分数较空白对照组大鼠升高（P〈0．05），SO2污染＋运动组大鼠升高更明显（P〈0．01）。结论SO2吸入和运动双重刺激作用下，大鼠心肌胶原纤维过度增生，胶原蛋白合成与降解失衡，从而影响心肌细胞间力的传递及心脏的正常舒缩功能。

英文摘要：

Objective To investigate the effects of sulfur dioxide（SO2） inhalation on the myocardial collagen fiber morphology and collagen content of exercising rats. Methods Twenty-four SD rats were randomly divided into four groups： rest group （RG）, exercise group （EG）, SO2 exposure rest group （SRG） and SO2 exposure exercise group （SEG）, six in each. The rats in SRG and SEG were put into the SO2 pollution environment. The rats in EG and SEG were trained in the motor driven wheel （8 m/min, 1 h/d for four consecutive weeks）. Myocardial hydroxyproline content （HVP） was tested by stomach acid solution enzyme, and then calculated collagen concentration. The collagenous volume fraction （CVF） of cardiac muscle and surrounding of small arteries was measured by medical image analysis system. Results Myocardial hydroxyproline content and collagen concentration of SEG, SRG and EG rats increased significantly （P〈0.05）; SEG elevated more significantly （P〈0.01）. Collagen content of cardiac muscle and around small arteries in EG rats elevated slightly （P〉0.05）; CVR of heart muscle and small arteries in SRG and SEG rats significantly increased compared with RG （P〈0.05）; SEG rats increased significantly （P〈0.01）. Conclusion SO2 and exercise cause myocardial collagen fiber in rats excessive proliferation, collagen synthesis and degradation will be in imbalance, which may have adverse effects on myocardial intercellular transfer in force and normal cardiac diastolic and constructional function.