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目的:探讨慢性心衰大鼠心肌细胞β2肾上腺素能受体(β2-AR)的表达变化,过表达β2-AR后心肌细胞收缩功能的改变及其可能机制。方法:通过腹主动脉缩窄术建立大鼠慢性心力衰竭(CCF)模型并采用胶原酶消化法分离心衰大鼠心肌细胞,转染携带β2-AR目的基因的重组腺病毒,通过免疫印迹方法检测正常细胞和心衰细胞β2-AR蛋白表达的变化,采用单个细胞动态边缘检测系统测定其收缩功能的改变。结果:与正常细胞相比,心衰时β2-AR蛋白的表达没有变化,转染β2-AR基因则使之表达增加(P<0.05)。与正常组相比,心衰组的基础收缩明显降低(3.955±1.684%vs5.472±2.918%,P<0.01);过表达β2-AR逆转了心衰心肌细胞的基础收缩(5.882±2.208%vs3.955±1.684%,n=60,P<0.01),但不影响心衰心肌细胞的最大收缩(9.366±2.646%vs9.066±3.509%)。结论:心衰时大鼠心肌细胞β2-AR的表达不变,但是其基础收缩功能降低,而β2-AR的过表达则能够改善心衰细胞的基础收缩功能。
Objective: To investigate the changes of β2-adrenergic receptor (β2-AR) expression in cardiomyocytes of chronic heart failure rats and the possible mechanism of myocardial contractile function after overexpression of β2-AR. Methods: The rat model of chronic heart failure (CCF) was established by abdominal aortic constriction. Cardiomyocytes were isolated by collagenase digestion and transfected with recombinant adenovirus carrying β2-AR gene. The changes of β2-AR protein expression in normal and heart failure cells were detected, and the change of contractile function was measured by single cell dynamic edge detection system. Results: Compared with normal cells, the expression of β2-AR protein did not change in heart failure, while the expression of β2-AR gene increased (P <0.05). Compared with the normal group, basal contraction of heart failure group was significantly lower (3.955 ± 1.684% vs 5.472 ± 2.918%, P <0.01); over-expression of β2-AR reversed the basic contraction of heart failure myocardial cells (5.882 ± 2.208% vs3.955 ± 1.684%, n = 60, P <0.01), but did not affect the maximal contraction of heart failure myocardial cells (9.366 ± 2.646% vs9.066 ± 3.509%). CONCLUSION: The expression of β2-AR in rat myocardial cells during heart failure is unchanged, but its basic contractile function is decreased. However, the over-expression of β2-AR can improve the basic contractile function of heart failure cells.