【摘要】 目的:观察在心力衰竭细胞上增加β1肾上腺素受体(β1-AR)表达对收缩功能的影响。方法:首先用异丙肾上腺素制作大鼠心力衰竭模型,然后分离、培养心肌细胞,转入含人β1-AR基因的腺病毒,24h后Westernblot检测细胞中β1-AR的含量,并进行单个心肌细胞收缩功能的分析。结果:心衰细胞上β1-AR含量为正常对照组的(0.56±0.19)倍(P<0.01),心力衰竭+转基因组β1-AR的含量为正常对照组的(5.68±0.36)倍(P<0.01);心力衰竭组心肌细胞对异丙肾上腺素刺激引起的收缩幅度较正常对照组明显降低(P<0.01),转入β1-AR基因后,可明显改善心力衰竭大鼠心肌细胞的收缩功能,选择性β1-AR拮抗剂CGP20712A可以完全阻断转入β1-AR后的效应,选择性β2-AR拮抗剂ICI118,551可以部分降低心力衰竭大鼠和β1-AR表达增加的心衰大鼠心肌细胞的收缩幅度。结论:在心力衰竭后的大鼠心肌细胞上增加β1-AR的表达,可改善细胞的收缩功能,这种作用可能是直接通过β1-AR实现的。β2-AR也参与了心力衰竭大鼠和β1-AR表达增加的心力衰竭大鼠心肌细胞的收缩功能。更多还原

【Abstract】 Objective:To observe the relationship between overexpressed β1-AR and the contractile amplitude in rat heart failure ventricular myocytes. Methods:Heart failure model was made with isoprenaline. Then,ventricular myocytes were isolated,cultured and infected with adenoviruses containing the sequence for human β1-adrenoceptor. The contents of β1-AR and the single ventricular myocytes contraction amplitudes were tested after the cells were infected with adenoviruses for 24 h. Results:The content in heart failure group was lower than that in control group. Overexpression of β1-AR markedly increased the content. The isoprenaline-stimulated contraction amplitudes in failure group were significantly lower than that in control group. Overexpression of β1-AR improved the contraction amplitudes. Selective β1-AR antagonist CGP20712A descended the isoprenaline-stimulated contraction amplitudes in heart failure myocytes infected with or without adenoviruses. Selective β2-adrenoceptor antagonist ICI118,551 partially decreased the contraction amplitude in heart failure myocytes infected with or without adenoviruses. Conclusion:The results suggested that overexpression of β1-AR increase the contraction amplitude in heart failure myocytes. The effect was directly related to β1-AR. β2-AR participated in the isoprenaline-stimulated contraction amplitudes.更多还原