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目的:观察12周有氧运动对慢性心力衰竭大鼠心功能、交感神经活性和运动能力的影响并探索其可能机制。方法:Wistar大鼠通过结扎冠状动脉建立心梗后心衰模型,术后4周后随机分为假手术安静组(SH组)、心梗安静组(MI组)和心梗运动组(MI-Ex组),MI-Ex组进行12周跑台运动,SH组和MI组保持安静状态。12周结束后,利用递增负荷跑台实验测定运动能力,包括力竭时间、力竭距离和最大跑速;超声心动图检测心脏结构与功能,包括左心室收缩末内径(LVESD)、左心室舒张末内径(LVEDD)、缩短分数(FS)、左室射血分数(LVEF)和心率(HR);高压液相色谱法测定心肌和血浆去甲肾上腺素(NE)水平;RT-PCR和Western Blot法检测心肌β1肾上腺素能受体(β1-AR)、G蛋白偶联受体激酶2(GRK2)和酪氨酸羟化酶(TH)基因和蛋白表达水平。结果:与SH组比较,MI组力竭时间、力竭距离和最大跑速均显著性降低(P<0.01);BW、FS和LVEF下降(P<0.01),HW、HW/BW、LVESD、LVEDD和HR升高(P<0.01);血浆NE升高,心肌NE降低(P<0.01);心肌β1-AR、TH m RNA和蛋白水平降低(P<0.01),GRK2 m RNA和蛋白水平升高(P<0.01)。与MI组比较,MI-Ex组力竭时间、力竭距离和最大跑速均显著性升高(P<0.01),LVESD和LVEDD降低(P<0.01),FS和LVEF升高(P<0.01);血浆NE降低,心肌NE升高(P<0.01);心肌β1-AR、TH m RNA和蛋白水平升高(P<0.01),GRK2 m RNA和蛋白水平降低(P<0.01)。结论:长期有氧运动增强慢性心衰大鼠心脏交感活性并改善心功能和运动能力,其机制可能与心肌GRK2表达下调以及β1-AR表达上调有关。
Objective: To observe the effects of 12-week aerobic exercise on cardiac function, sympathetic nerve activity and exercise capacity in rats with chronic heart failure and to explore its possible mechanism. Methods: Wistar rats were established by heart ligation of coronary artery after heart failure model, 4 weeks after the surgery were randomly divided into sham operation group (SH group), MI group (MI group) and myocardial infarction group (MI- Ex group). The treadmill exercise was performed in MI-Ex group for 12 weeks, and the SH and MI groups remained quiet. At the end of 12 weeks, treadmill exercise was used to determine exercise capacity, including exhaustion time, exhaustive distance and maximum running speed; echocardiography was used to measure cardiac structure and function, including left ventricular end systolic diameter (LVESD), left ventricular diastolic (LVEDD), fractional shortening (FS), left ventricular ejection fraction (LVEF) and heart rate (HR). The myocardial and plasma levels of norepinephrine (NE) were measured by high pressure liquid chromatography (Β1-AR), G protein-coupled receptor kinase 2 (GRK2) and tyrosine hydroxylase (TH) gene and protein expression were detected by immunohistochemistry. Results: Compared with SH group, the exhaustion time, exhaustive distance and maximum running speed in MI group were significantly decreased (P <0.01); BW, FS and LVEF decreased (P <0.01); HW, HW / BW, LVESD, LVEDD and HR increased (P <0.01), NE increased, NE decreased (P <0.01), myocardial β1-AR, TH m RNA and protein levels decreased (P <0.01) High (P <0.01). Compared with MI group, the exhaustion time, exhaustive distance and maximal running speed in MI-Ex group were significantly increased (P <0.01), LVESD and LVEDD decreased (P <0.01), FS and LVEF increased (P <0.01). The levels of β1-AR, TH m RNA and protein in myocardium were increased (P <0.01) and GRK2 m RNA and protein levels were decreased (P <0.01). CONCLUSION: Long-term aerobic exercise can enhance cardiac sympathetic activity and improve cardiac function and exercise capacity in chronic heart failure rats. The mechanism may be related to the down-regulation of GRK2 expression and the up-regulation of β1-AR expression.