抄録
1) In isolated canine ventricular myocardium, automaticity could be induced by a passage of small depolarizing DC-currents. The mechanism was attributed to inflowing Ca++ and Na+ currents and time-dependent deactivation of outward K+ current under a condition of high membrane resistance due to anomalous rectification. Significance of the automaticity was discussed in relation to the ventricular arrhythmias encountered in very early stage of myocardial infarction. 2) In in situ canine hearts, chlorpromazine induced time (preceding cycle length)-dependent decrease in conduction velocity within the ventricle. Thus QRS-duration of non-premature beats was lengthened at rapid pacing rates while QRS-duration of atrial premature beats was lengthened also at short coupling intervals in the drug-treated dogs. These slow conductions were not due to reduced take-off potential of action potentials but due to drug-induced slow recovery of rapid Na+ system. The phenomenon may be responsible for reported QRS-prolongation and fatal ventricular arrhythmias encountered in the patients receiving phenothiazines.
