Luna-Ortiz Pastor, Zarco-Olvera Gabriela, Ramírez-Ortega Margarita, Tenorio-López Fermin A, Gutiérrez Alfonso, Martínez-Rosas Martín, Del-Valle Mondragón Leonardo, Pastelín Gustavo
Departamento de Farmacología, Instituto Nacional de Cardiología Ignacio Chávez, México.
Arch Cardiol Mex. 2009 Jul-Sep;79(3):182-8.
To study the antiarrhythmic effect of remifentanil in experimental arrhythmias in dogs.
We used dogs weighing 12 kg-18 kg anesthetized with 30 mg/kg sodium pentobarbital given intravenously. Ventricular arrhythmia, ventricular fibrillation and death were induced with digoxin (9 microg/kg/min). In another model, two types of arrhythmia were induced in the right atrium, one of them with aconitine crystals placed on the right atrium and the other was induced in the basement of the right atrium by electrical stimulation. The potential antiarrhythmic action of remifentaniL was investigated in ventricular and atrial arrhythmias by the administration of an intravenous bolus after toxic signs were evident. Thus, two arrhythmias with different mechanisms were generated. Leads DII, unipolar left intraventricular and right atrial leads, and left ventricular pressure were used to record control tracings and tracings in presence of remifentanil, during ventricular arrhythmia.
Remifentanil abolished toxic effects of digoxin, it eliminated the A-V dissociation and ventricular extrasystoles, reverting to sinus rhythm in each case. Remifentanil extended the time to reach lethal doses from 63.25 +/- 11.3 to 100 +/- 11.8 min. These effects were blocked by naloxone (0.01 microg/kg) applied before remifentanil. In the two arrhythmias model, remifentanil suppressed both, ectopic focus and atrial flutter.
Remifentanil elicits antiarrhythmic and cardioprotective effects in experimental ventricular arrhythmias induced by digoxin and in a model of two atrial arrhythmias induced by aconitine and by electrical stimulation.
研究瑞芬太尼对犬实验性心律失常的抗心律失常作用。
选用体重12 kg - 18 kg的犬，静脉注射30 mg/kg戊巴比妥钠进行麻醉。静脉注射地高辛（9微克/千克/分钟）诱发室性心律失常、心室颤动和死亡。在另一个模型中，在右心房诱发两种心律失常，一种是将乌头碱晶体置于右心房诱发，另一种是通过电刺激在右心房底部诱发。在中毒症状明显后静脉推注给药，研究瑞芬太尼在室性和房性心律失常中的潜在抗心律失常作用。因此，产生了两种机制不同的心律失常。在室性心律失常期间，使用Ⅱ导联、单极左心室内导联和右心房导联以及左心室压力来记录对照描记图和瑞芬太尼存在时的描记图。
瑞芬太尼消除了地高辛的毒性作用，消除了房室分离和室性期前收缩，每种情况下均恢复为窦性心律。瑞芬太尼将达到致死剂量的时间从63.25±11.3分钟延长至100±11.8分钟。这些作用在瑞芬太尼给药前应用纳洛酮（0.01微克/千克）后被阻断。在两种心律失常模型中，瑞芬太尼均抑制异位起搏点和心房扑动。
瑞芬太尼在由地高辛诱发的实验性室性心律失常以及由乌头碱和电刺激诱发的两种房性心律失常模型中具有抗心律失常和心脏保护作用。
