Introduction and objective: To study the action of adenosine in experimental ventricular tachycardia.
Material and method: We studied 173 mongrel dogs weighing 13-17 kg anesthetized with 30 mg/kg sodium pentobarbital given intravenously. Myocardial lesions were provoked with the injection of 1-1.5 mL phenol in the free wall of the left ventricle. Ventricular arrhythmia was induced 30 min later with aconitine crystals inserted into the periphery of the damaged area. The potential early and delayed antiarrhythmic action of adenosine was systematically investigated in 85 animals. Leads DII, aVR and aVL, unipolar right and left intraventricular leads, and one unipolar lead on the wall of the superior vena cava were used to record control tracings and tracings in the presence of myocardial damage during ventricular tachycardia and after injection of the drug.
Results: Sinus rhythm did not reappear in 72 control animals that did not receive adenosine. In the 63 animals with aconitine-induced ventricular tachycardia associated to myocardial damage, the optimal response to 6 mg adenosine-early and fleeting sinus rhythm-was seen in 45% of the dogs; delayed sinus rhythm was seen in 5%. In 67% of the 18 animals with ventricular tachycardia due only to myocardial damage, early and late sinus rhythm appeared with doses of 6 and 12 mg, and late sinus rhythm was seen with a dose of 12 mg.
Conclusions: The antiarrhythmic action of adenosine was seen not only in ventricular tachycardia due to aconitine (triggered activity), but also in tachycardia induced by the myocardial damage (microreentries).