Suwalsky M, Villena F
Faculty of Chemical Sciences, University of Concepción, Chile.
Cell Mol Biol (Noisy-le-grand). 1995 Mar;41(2):307-12.
Several hypotheses suggest that the molecular mechanism of action of class I antiarrhythmic drugs (AAD) involve non-specific interactions of these compounds with phospholipid bilayers of the myocardial membrane that surround and functionally modulate ion transport by sodium channels. As a result of these interactions the channel function would be altered. To probe the validity of these hypotheses three AAD with different degrees of lipophilicity were made to interact in vitro with human erythrocytes in a wide range of concentrations. The most lipophilic drug was asocainol (ASOC), the least one was procainamide (PROC) while the lipophilicity of the third, quinidine (QUIN), lay somewhere between the other two. The observations made by scanning electron microscopy (SEM) showed that the three AAD produced profound shape alterations to the incubated erythrocytes. However, the type and intensity of these changes were dependent on the drug under study and its concentration.
有几种假说认为，I类抗心律失常药物（AAD）的分子作用机制涉及这些化合物与心肌膜磷脂双层的非特异性相互作用，心肌膜围绕钠通道并在功能上调节离子转运。这些相互作用的结果是通道功能会发生改变。为了探究这些假说的正确性，使三种具有不同亲脂性程度的AAD在体外与不同浓度范围内的人红细胞相互作用。亲脂性最强的药物是阿索卡诺（ASOC），亲脂性最弱的是普鲁卡因胺（PROC），而第三种药物奎尼丁（QUIN）的亲脂性介于另外两种药物之间。通过扫描电子显微镜（SEM）进行的观察表明，这三种AAD使孵育后的红细胞发生了显著的形态改变。然而，这些变化的类型和强度取决于所研究的药物及其浓度。
