[Mechanisms of the anomalous activity of the Purkinje fibers in the late stage of experimental myocardial infarct in dogs].

The anomalously active (AA) subendocardial Purkinje's fibers (PF) in the ischemic zone 24 hours after occlusion of the left descending coronary artery (LDCA) in dogs are proposed to be divided into 2 groups according to their reaction to the changes in the ionic composition of perfusion solution. The AAPF frequency in the first group decreased by increase in [Ca2+]o, increased by fall in [Ca2+]o and was proportional to [Na+]o. In the second group AAPF frequency rose under actions increasing [Ca2+]i (increase in [Ca+]o, decrease in [Na+]o), and fell under actions reducing [Ca2+]i (decrease in [Ca2+]o, increase in [Na+]o). After short-term (10 s) high frequency stimulation the AAPF frequency in the group I fibers either remained unchanged or insignificant transitory slowing down was registered. In the group II fibers the AA frequency after high frequency stimulation either remained unchanged or insignificant transitory elevation was observed. The anomalous activity in the group I fibers could be blocked by tetrodotoxin, while verapamil was practically ineffective. In the second group anomalous activity was blocked by both drugs. We conclude thus that one day after the occlusion of LDCA in the ischemic zone PF with anomalous activity caused by anomalous automaticity as well as by trigger mechanism may be present. The pacemaker current inducing anomalous automaticity is possibly caused by Na+ intake through ischemically modified natrium channels.