Mészáros J, Kelemen K, Kecskeméti V, Kovács G
Arch Int Pharmacodyn Ther. 1986 Mar;280(1):84-96.
The effect of quinidine (class 1 agent) and verapamil (class 4 agent) on the adenosine-induced changes in the electrical and mechanical activity of the left atrial myocardium of guinea-pig was studied. Adenosine alone shortened the action potential duration, slightly hyperpolarized the membrane and increased the Vmax as well as induced a negative inotropic effect. Quinidine, a membrane-stabilizing drug, prolonged the action potential duration, decreased the Vmax, and increased the contractile force, i.e. diminished the electrical and mechanical changes in the atria treated with adenosine. These effects became more pronounced in the presence of aminophylline, a P1-purinoceptor blocker. In contrast, verapamil, a Ca-channel blocker, enhanced the adenosine-induced shortening in the early repolarization phase of the action potential, and the negative inotropic effect. This action of verapamil could be attenuated with aminophylline. The results suggest that adenosine can influence the effect of antiarrhythmics compounds and vice versa, and that the action of adenosine is possibly mediated via interaction with an extracellular P1-purinoceptor.
研究了奎尼丁(Ⅰ类药物)和维拉帕米(Ⅳ类药物)对腺苷诱导的豚鼠左心房心肌电活动和机械活动变化的影响。单独使用腺苷可缩短动作电位时程,使膜轻度超极化,增加最大上升速率,并产生负性肌力作用。奎尼丁作为一种膜稳定药物,可延长动作电位时程,降低最大上升速率,并增加收缩力,即减弱了腺苷处理的心房中的电和机械变化。在P1嘌呤受体阻滞剂氨茶碱存在时,这些效应变得更加明显。相比之下,维拉帕米作为一种钙通道阻滞剂,增强了腺苷诱导的动作电位早期复极化阶段的缩短以及负性肌力作用。维拉帕米的这种作用可被氨茶碱减弱。结果表明,腺苷可影响抗心律失常化合物的作用,反之亦然,且腺苷的作用可能是通过与细胞外P1嘌呤受体相互作用介导的。