Seipel L, Hoffmeister H M
Department of Cardiology, Medical Hospital, University of Tuebingen, Germany.
Eur Heart J. 1993 Nov;14 Suppl H:36-40. doi: 10.1093/eurheartj/14.suppl_h.36.
The inotropic effects of sotalol in comparison to other antiarrhythmic drugs were tested in an experimental model allowing isovolumic measurements independently of the loading conditions. All class I drugs had a similar negative inotropic effect. d,l-Sotalol caused a dose-dependent depressant effect on the rate of left ventricular pressure development. The same held true for l-sotalol. In contrast, d-sotalol, in clinical doses, revealed no significant inotropic effects in normal hearts. In a postischemic model, d-sotalol led to a further deterioration of left ventricular function. It could be demonstrated by autonomic blockade that this effect was mainly the result of the remaining weak beta-blocking activity of the d-isomer in addition to its class III action. After intravenous administration of amiodarone in doses of 10 mg.kg-1, no significant inotropic effects were found in normal rats.
在一个可独立于负荷条件进行等容测量的实验模型中,测试了索他洛尔与其他抗心律失常药物相比的变力作用。所有I类药物都有类似的负性变力作用。消旋索他洛尔对左心室压力上升速率产生剂量依赖性的抑制作用。左旋索他洛尔也是如此。相比之下,临床剂量的右旋索他洛尔在正常心脏中未显示出明显的变力作用。在缺血后模型中,右旋索他洛尔导致左心室功能进一步恶化。自主神经阻断实验表明,这种作用主要是由于右旋异构体除了其III类作用外,仍具有较弱的β受体阻断活性。给正常大鼠静脉注射10mg.kg-1剂量的胺碘酮后,未发现明显的变力作用。