摘要：
Objective To investigate the effects of metoprolol on β-AR-AC-cAMP pathway and ventricular stability in stressed rabbit model .Methods Thirty male rabbits were randomly divided into control group ( n =10 ) , stressed group ( n =10 ) , stressed plus metoprolol treatment group ( n =10 ) .Complex stimulations of sound and electricity for 24 hours were used to establish acute stressed model .To detect ventricular fibrillation induce rate in each group , we measured the ser-um epinephrine(E), norepinephrine(NE)in the rabbit serum and evaluated the myocardial β-adrenergic receptor (β-AR) density, adenylate cyclase (AC) activity and cyclic adenosine monophosphate (cAMP) levels in ventricular tissues.Results Ventricular fibrillation induce rate in stressed group was significantly higher than control group (χ2 =6.270, P =0.012), the induce rate in treatment group was lower than stressed group (χ2 =9.600, P =0.002),but there was no difference be-tween and treatment group control group (χ2 =0.457, P =0.499).Serum E, NE were higher in stressed group compared to control group ( q =22.49, P <0.01;q =33.64, P <0.01), and were lower in treatment group compared to stressed group ( q =6.45, P <0.01;q =9.76, P <0.01).Ventricular AC activity and cAMP were higher in stressed group compared to control group ( q =34.70, P <0.01;q =11.74, P <0.01), and were lower in treatment group compared to stressed group ( q =21.61, P <0.01;q =4.52, p =0.004).Ventricular β-AR density was significantly higher in stressed group com-pared to control group ( q =8.36, P <0.01), but no significant differences were found between treatment group and stressed group (q =2.21, p =0.129).Equilibrium dissociation constants (KD values) are also appealed no significant difference among these three groups ( F =1.096, P =0.349).Conclusion By inhibiting the β-AR-AC-cAMP signal transduction pathway and inhibiting the sympathetic excitation , decreasing of NE and E release , and improve the stability of the ventricle .%目的：观察美托洛尔对应激家兔β-AR-AC-cAMP信号转导通路和心室稳定性的影响及其作用机制。方法2014年2月—2015年9月于哈尔滨医科大学附属第一医院心内科实验室进行实验。雄性家兔30只，随机分为对照组（ n ＝10）、应激组（ n ＝10）、干预组（给予美托洛尔， n ＝10），应激组和干预组采用声、电复合持续刺激24 h，建立急性应激模型。建模后麻醉开胸电生理检测各组室颤诱发率，观测血清肾上腺素（E）、去甲肾上腺素（NE），检测心肌细胞β肾上腺素能受体（β-AR）密度、腺苷酸环化酶（ AC）活性和环磷酸腺苷（ cAMP）水平。结果应激组室颤诱发率高于对照组（χ2＝6．270， P ＝0．012）和干预组（χ2＝9．600， P ＝0．002），对照组与干预组比较无显著差异（χ2＝0．457， P ＝0．499）。应激组血清E和NE含量均高于对照组（ q ＝-22．49、－33．64， P ＜0．01）和干预组（ q ＝－6．45、－9．76， P ＜0．01）；应激组心室肌AC、cAMP水平均高于对照组（ q ＝－34．70、－11．74， P ＜0．01）和干预组（ q ＝－21．61、－4．52， P ＝0．004）。应激组、干预组心室肌β-AR密度均高于对照组（ q ＝-8．36、－6．14， P ＜0．01），但干预组和应激组间β-AR密度差异无统计学意义（ q ＝-2．21， P ＝0．129），3组平衡解离常数（KD 值）差异无统计学意义（ F ＝1．096， P ＝0．349）。结论美托洛尔通过抑制｀β-AR-AC-cAMP信号转导通路，抑制交感兴奋，减少NE和E释放，提高心室稳定性。
