Bartosová Ladislava, Novák Filip, Frydrych Marek, Parák Tomás, Opatrilová Radka, Brunclík Vít, Kolevská Jana, El Moataz Elnaggar, Necas Jirí
Department of Human Pharmacology and Toxicology, University of Veterinary and Pharmaceutical Sciences, 612 42 Brno, Czech Republic.
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2005 Dec;149(2):339-43.
The anti-arrhythmic effect was tested on the model of aconitine-induced arrhythmia. The experiment was performed in vivo with 31 male Wistar laboratory rats. Group A was first administered aconitine and, after the onset of the first sinus rhythm disorders, the 44Bu compound was administered. Group B was first administered the 44Bu compound and only after that the aconitine. The control group was administered aconitine and saline as a replacement of the tested compound. In group A, there was a decrease in the ventricular fibrillation occurrence from 100 % to 8 % (p < 0.001) after the administration of the 44Bu compound. In the B group, the onsets of all monitored arrhythmia types were delayed by an average of 15.6 min. Ventricular rhythm occurrence was decreased from 100 to 20 %, as well as ventricular fibrillations, from 100 to 0 % (p < 0.001).
在乌头碱诱导的心律失常模型上测试抗心律失常作用。实验在31只雄性Wistar实验大鼠体内进行。A组先给予乌头碱，在首次窦性心律紊乱出现后，给予44Bu化合物。B组先给予44Bu化合物，之后才给予乌头碱。对照组给予乌头碱并用生理盐水替代受试化合物。在A组，给予44Bu化合物后，室颤发生率从100%降至8%（p<0.001）。在B组，所有监测到的心律失常类型的发作平均延迟15.6分钟。室性心律发生率从100%降至20%，室颤发生率从100%降至0%（p<0.001）。
