Aseptic occlusion of the anterior descending artery in dogs leads to ectopic ventricular tachycardia after a latency of 4.5 to 8 hours, persisting for 2 to 4 days.
Experimental coronary occlusion in dogs demonstrates a delayed onset of ventricular tachycardia that correlates with the time required for histologic necrosis.
Following aseptic occlusion of the anterior descending artery of the dog's heart ectopic ventricular tachycardia develops after a latency of four and one-half to eight hours, and persists for two to four days. Large gross infarcts are found in all hearts. The duration of latency of onset of major ectopic activity approximates the minimal period of ischemia required to produce histologic signs of necrosis. It is suspected that products or processes of necrosis have excitatory effects on tissues bounding the ischemic zone. Evidences concerning various possible excitatory factors are briefly reviewed.
A. Sidney Harris (1950) studied Experimental Coronary Occlusion. Aseptic occlusion of the anterior descending artery was evaluated on Development of ectopic ventricular tachycardia. Aseptic occlusion of the anterior descending artery in dogs leads to ectopic ventricular tachycardia after a latency of 4.5 to 8 hours, persisting for 2 to 4 days.
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