【作者】 彭继平；

【导师】 曾庆华；

【作者基本信息】 东北师范大学 ， 生理学， 2007， 硕士

【摘要】 运动性疲劳指机体不能将它的机能保持在某一特定水平,或者不能维持某一预定的运动强度[1]。运动性疲劳对心脏功能影响研究虽然有报道,但其影响作用及机制仍然不清楚,尤其是在分子细胞水平上对心肌细胞内[Ca²⁺]i的研究没有报道,因此本论文通过游泳训练制备运动性疲劳大鼠模型,检测心肌细胞钙离子浓度的变化,探讨运动性疲劳对心脏功能的影响。本文研究了心肌细胞内[Ca²⁺]i变化的规律,血液生化,心电,心肌力学相关指标的变化及人参皂苷单体Rb1对心肌的保护作用,这对人们的健康及长期疲劳心肌钙水平调控控制范围具有重要的理论意义和现实意义。通过连续15天,每天3小时的游泳耐力运动建立大鼠运动性疲劳模型,大鼠疲劳时游泳水淹过鼻,且经常下沉。应用自动生化分析仪器测定血浆乳酸脱氢酶,肌酸磷酸激酶,葡萄糖,Ca²⁺变化。应用Power Lab测定标Ⅱ导联心电图（ECG）,在体左心室收缩压,左室舒张末期压,室内最大升降速率,心率。为了排除神经和体液因素的影响,应用Langendorff离体灌流测定左心室收缩压,左室舒张末期压,室内最大升降速率,心率。并在细胞水平上应用绝对钙离子成像技术测定了心肌细胞[Ca²⁺]i。运动性疲劳可使大鼠血浆CK由对照组的357.83±50.45IU/L显著上升至558.1±101.2IU/L （P<0.01）,升高55.97%; Glu由对照组的7.63±1.62mmol/L显著升高至10.28±2.08mmol/L （P<0.05）,升高34.67%;Ca²⁺由对照组的2.57±0.05mmol/L显著下降至2.21±0.11mmol/L（P<0.01）,降低13.9%。过量运动性疲劳可使大鼠心脏显著增大,引起心肌肥厚,肌结构重组。心脏重量由0.573±0.03g显著增重至疲劳后的1.049±0.08 （P<0.01）,增重82.89%运动性疲劳可使大鼠心电R波幅值显著增大,由0.5012±0.05mv增至0.9072±0.3152mv（P<0.01）,增幅81.01%。运动性疲劳可使大鼠心肌力学指标较正常大鼠显著升高。在体LVSP显著升高,由15.88±0.47kPa增至18.14±0.19kPa （P<0.01）,增幅14.24%;+dp/dt显著升高（P<0.05）,增加了45.32%。对离体心脏,LVSP运动性疲劳组（5.681±0.497kPa）显著高于（P<0.01）正常组（4.539±0.389kPa）,高出25.17%;+dp/dt显著升高（P<0.05）,增加了30.78%。对心肌细胞,运动性疲劳可导致细胞内[Ca²⁺]i显著升高,由正常的107.77±27.04nM上升至308.58±69.48nM,升高了186.3%。人参皂苷单体Rb1可使运动性疲劳大鼠血浆CK的升高回复至292±63.89IU/L（P<0.01） ,下降47.68% ; Rb1可使Glu进一步上升至14.85±3.73mmol/L（P<0.05）,上升44.46%; Rb1可使运动性疲劳引起的Ca²⁺下降回升至2.47±0.08mmol/L （P<0.01）,回升11.61%。运动性疲劳使大鼠血浆中Ca²⁺浓度降低,肌细胞内Ca²⁺增加,Rb1能有效提高血浆中Ca²⁺浓度,而起到阻滞Ca²⁺向细胞内流,减缓细胞钙超载的作用。Rb1对运动性疲劳引起的R波幅值降低不明显。人参皂苷单体Rb1可降低运动性疲劳大鼠心肌收缩力,对心肌起到保护作用。Rb1可使运动疲劳引起的LVSP上升回复至16.41±0.43kPa,下降9.53%; Rb1可使+dp/dt升高显著回复（P<0.01）,下降了40.34%。对离体心脏,Rb1可极显著的降低运动性疲劳大鼠LVSP（2.737±0.595kPa）,降低51.83%;Rb1极显著（P<0.01）的降低了+dp/dt,下降了46.53%。Rb1对正常组心肌也具有负性肌力效应,作用效果不如疲劳组明显。应用Ca²⁺通道阻滞剂维拉帕米（Varapamil）做阳性对照,对疲劳组心肌也具有与Rb1相似的效果,作用更为明显,但可使心率显著降低。运动性致疲劳可使大鼠心肌收缩力增强,心脏体积增大,心肌肥厚使得心功能增强,使大鼠血浆中Ca²⁺浓度降低,心肌细胞内[Ca²⁺]i升高。Rb1能有效提高血浆中Ca²⁺浓度,而起到阻滞Ca²⁺向细胞内流,减缓细胞钙超载的作用,Rb1可降低运动性疲劳大鼠心肌的收缩力,对心肌起到保护作用。更多还原

【Abstract】 Exercise induced fatigue is body can’t keep its physiological process on an order level or can’t keep on certain sports strength. To study the mechanism of exercise induced fatigue and medical health care support improve the exercise ability and fatigue resume has a very important theory, practice, society benefit for improving exercise achievement and keeping fit. Take the data of [Ca²⁺]i in myocardial cells, plasma biochemical indices, the apparent of heart, ECG and myocardium mechanics to explore the effect of exercise induced fatigue on rats’heart function. And then study the anti-exercise fatigue function of ginsengnoside Rb1, which can scavenge oxygen free radicals, improve the activity of SOD, block cell calcium channel opening.The exercise-induced fatigue models in rats were established by 15 days chronic swimming training. Using the automatic biochemical analysis instruments to take the data of plasma biochemical indices; take the standardⅡ-lead ECG; take the data of myocardium mechanics in vivo and vitro; and using the ion imaging technique to measure [Ca²⁺]i in mycardial cells.Exercise-induced fatigue made the CK of rats blood plasma increased from 357.83±50.45IU/L to 558.1±101.2IU/L （P<0.01）, increased 55.97%; Glu increased from 7.63±1.62mmol/L to 10.28±2.08mmol/L （P<0.05）, increased 34.67%; Ca²⁺ decreased from 2.57±0.05mmol/L to 2.21±0.11mmol/L（P<0.01）, decreased 13.9%. Exercise-induced fatigue made rats’heart increased obviously and myocardial hypertrophy. The weight of rats’heart increased from 0.573±0.03g to 1.049±0.08 （P<0.01）, increased 82.89%. Exercise-induced fatigue made rats’ECG R wave increased rapidly from 0.5012±0.05mv to 0.9072±0.3152mv（P<0.01）, increased 81.01%. Exercise-induced fatigue made rats’myocardium mechanics much higher than control. In vivo, exercise- induced fatigue, LVSP increased from 15.88±0.47kPa to 18.14±0.19kPa （P<0.01）, increased 14.24%; +dp/dt increased obviously （P<0.05）, increased 45.32%. In vitro, LVSP in Exercise-induced fatigue（5.681±0.497kPa） was much higher than control （4.539±0.389kPa, P<0.01）, 25.17% higher; +dp/dt increased obviously （P<0.05） in exercise-induced fatigue rats, increased 30.78%. The [Ca²⁺]i in fatigue myocardial cells （308.58±69.48nM） are much higher than control （107.77±27.04nM）.Ginsengnoside Rb1 can make the CK rise of exercise-induced fatigue rats blood plasma decrease to 292±63.89IU/L（P<0.01）, decreased 47.68%; Rb1 can make Glu increased more to 14.85±3.73mmol/L（P<0.05）, increased 44.46%; Rb1 can make it recover to 2.47±0.08mmol/L （P<0.01）, increased 11.61%. Exercise-induced fatigue can reduce blood plasma Ca²⁺ concentration, enhance in-cell Ca²⁺ concentration, and Rb1 can increase blood plasma Ca²⁺ concentration, decrease in-cell Ca²⁺ concentration, delay cell calcium overload. Rb1 did little to decrease R wave in exercise-induced fatigue rats. Ginsengnoside Rb1 decreased myocardium mechanicals in fatigue rats, and protect cardiac muscle. In vivo, exercise- induced fatigue, Rb1 recovered LVSP to 16.41±0.43kPa（P<0.01）, decreased 9.53%; Rb1 also recovered +dp/dt（P<0.01）, decreased 40.34%. In vitro, Rb1 can reduce LVSP rapidly to 2.737±0.595kPa （P<0.01）, reduced 51.83%; Rb1 decreased +dp/dt rapidly too（P<0.01）, decreased 46.53%. Rb1 also has the negative myocardium mechanics in control, but not significant to fatigue. Varapamil has similar effect on fatigue hearts, and more effective, but it reduced heart rate notably.Exercise-induced fatigue rats have higher myocardium mechanics, bigger heart, and get myocardial hypertrophy. Exercise-induced fatigue can reduce blood plasma Ca²⁺ concentration, enhance in-cell Ca²⁺ concentration in myocardial cells. Rb1 can increase blood plasma Ca²⁺ concentration, decrease in-cell Ca²⁺ concentration, delay cell calcium overload. Rb1 can decrease the myocardium mechanics of exercise-induced fatigue rats and play a positive role on cardiac protective, it shows fewer negative affection compare with Varapamil.更多还原