β_2受体阻断药降低梗死后心肌细胞环磷腺苷的含量

The effects of beta 2-adrenergic receptor blocker on introcellular cAMP level in ventricular myocytes after myocardial infarction

目的研究心肌梗死后2-8周心肌细胞β2受体对环磷腺苷(adenosine cyclophosphate,cAMP)含量影响的动态变化,探讨心肌梗死后β2受体在交感神经激动作用中所占地位。方法Wistar大鼠20只随机分为:正常对照组、心肌梗死后2周组、4周组、8周组。分离心肌细胞,每组制备35份样品,按给药不同随机分为7小组,用酶联免疫方法测定心肌细胞环磷腺苷含量。结果在正常和梗死后2、4、8周心肌细胞,β2受体激动可使心肌细胞环磷腺苷含量(pmol／105 cells)分别升高98％、134％、148％和151％(P<0．05)。心肌梗死后,选择性β2受体阻断药对β受体激动引发的心肌细胞环磷腺苷含量的抑制程度增高,选择性β1受体阻断药对其的抑制程度下降,非选择性β受体阻断药对β受体激动引发的正常和心肌梗死后心肌细胞环磷腺苷含量升高均能抑制。结论心肌梗死后β2受体在β受体激动引发的心肌细胞环磷腺苷含量升高作用中所占比例升高。心肌梗死后β2受体在交感神经激动产生的正性肌力和正性变时作用中地位可能提高。

Objectives To investigate the effects of β2-AR on adenosine cyclophosphate（cAMP） content in infarcted heart. Methods Twenty adult Wistar rats were divided into four groups at random： the control group, the two weeks, four weeks and eight weeks post-myocardial infarction groups. The chest of rat was opened and a ligature was placed around the left anterior descending coronary artery. Rats in control group were sham-operated without the coronary artery ligation. After the operation, rats were fed for two, four or eight weeks respectively. Myocytes were enzymatically disassociated by Langedorff perfusion. The cAMP content was determined by competitive enzyme immunoassay. Results β2-AR agonist increased cAMP content of the control group and the two weeks, four weeks and eight weeks post-MI groups to 98%, 134%, 148% and 151% of blank levels respectively （P 〈 0.05）. β2-AR antagonist attenuated the rise of cAMP content induced by β2-AR agonist more strongly in myocytes from post-MI hearts than in controls, whereas β2-AR antagonist is opposite to β2-AR antagonist. Conclusions The effects of β2-AR on cAMP content in myocytes were stronger after MI. It suggested that β2-AR might be more important in the inotropic action and positive chronotropic action induced by sympathetic drive.