VENTRICULAR FIBRILLATION INDUCED BY CORONARY OCCLUSION DURING HYPOTHERMIA IN DOGS AND THE EFFECTS OF QUINIDINE, QUINACRINE, AND OXYTOCIN

In dogs under pentobarbitone anesthesia, acute occlusion of the anterior descending branch of the left coronary artery at normal body temperature induced ventricular fibrillation in 30% of the animals, while hypothermia by surface cooling led to fibrillation in 40% of the animals. On the other hand, temporary coronary occlusion with hypothermia at 23 °C oesophageal temperature invariably induced ventricular fibrillation (15 experiments) within an average of 5.4 minutes of occlusion. Prior injections of quinidine and quinacrine protected 40 and 70%, respectively, of the dogs against this type of ventricular fibrillation (10 experiments each). Oxytocin (1–2 i.u./kg) offered no protection (six experiments) nor did it reverse established fibrillation under these conditions. It is concluded that temporary coronary artery occlusion at 23 °C oesophageal temperature in dogs is an effective and consistent method of producing ventricular fibrillation. It is also postulated that reduction of the coronary blood supply to the heart might be a precipitating factor in hypothermic ventricular fibrillation in surgery.