为了观察SO2污染环境下运动对大鼠心功能的影响,从心脏局部肾素-血管紧张素系统(renin-angiotensin system,RAS)核心成员---血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)Ⅰ型受体(AT1 R)介导的心肌胶原纤维形态结构重塑的角度出发,应用心脏插管技术观察大鼠的心脏功能;采用放射免疫技术(ELISA)、免疫组织化学和胃酶酸解法等方法对心肌局部ρ(AngⅡ)、AT1 R蛋白表达水平、w(HYP)(HYP为羟脯氨酸)及胶原容积分数进行检测.结果表明:①单纯运动组(EG)大鼠主动脉收缩压、左室内压峰值、±dp∕dtmax(左室内压最大上升速率∕下降速率)显著升高(P<0.01),舒张压、AT1R蛋白表达显著降低(P<0.01),w(HYP)、w(CC)(心肌胶原浓度)、PVCA(血管周围胶原面积)、CVF(心肌胶原容积分数)及ρ(AngⅡ)有升高趋势(P>0.01);②单纯SO2污染组(SRG)大鼠左室末期舒张压显著升高(P<0.01),左室内压±dp∕dtmax显著降低(P<0.01);w(HYP)、w(CC)、PVCA、CVF、ρ(AngⅡ)及AT1 R蛋白表达水平均显著升高(P<0.01);③SO2污染+运动组(SEG)大鼠左室末期舒张压显著升高(P<0.01),主动脉收缩压、左室内压峰值、左室内压±dp∕dtmax显著降低(P<0.01),w(HYP)、w(CC)、PVCA、CVF、ρ(AngⅡ)及AT1R蛋白表达水平均显著升高(P<0.01),并且较SRG大鼠升高更显著(P<0.01).研究显示,SO2污染导致运动大鼠心肌胶原纤维形态结构发生异常重塑,最终使大鼠的心功能产生显著的负性变力性效应,其机制可能与心脏局部RAS系统的激活有关.%To observe the effects of SO2 pollution on rats'heart function, from the point of view of the core members of angiotensin Ⅱ of cardiac local renin-angiotensin system ( RAS) mediated morphological remodeling of myocardial collagen fibers, cardiac function was observed by cardiac intubation technology. The levels of Ang Ⅱ, AT1 R protein expression, hydroxyproline content and collagen volume fraction were measured by radioimmunoassay ( ELISA ) ;immunohistochemistry and gastric acid hydrolysis. The results showed that:( 1) Appropriate exercise to adapt to the myocardial collagen fibers in the morphological structure of adaptive remodeling, and to enhance myocardial contractility, showed that compared with RG, the LVSP, SBP and ±dp∕dtmax of the rats in EG increased significantly (P<0. 01);the expression of DBP and AT1R protein levels were significantly decreased (P<0. 01);and the contents of HYP, CC, PVCA, CVF and Ang Ⅱ increased, but the difference was not significant (P>0. 01). (2) SO2 inhalation caused abnormal remodeling of myocardial collagen fibers in rats, and reduced myocardial contractility, as shown by the facts that the LVEDP of rats in SRG increased significantly ( P<0. 01); ± dp∕dtmax significantly decreased (P<0. 01); and the contents of myocardial HYP, CC, PVCA, CVF and Ang Ⅱ and its receptor AT1R protein expression levels were significantly higher (P<0. 01). (3) SO2 inhalation and exercise caused rat myocardial collagen fiber hyperplasia, and ultimately made the rats' cardiac function produce significant negative force effect, as shown by the fact that EVF SBP, LVSP and ±dp∕dtmax were significantly decreased ( P<0. 01). SO2 pollution brings myocardial collagen fibers hyperplasia in exercised rats and imbalance of collagen synthesis and degradation, and thus affects the transmission force of the myocardial cells, leading to significant negative inotropic effect in rats'cardiac systolic function. The mechanism might be related to the activation of the local RAS system.
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