Why the study?
Do depolarizing currents and chlorpromazine induce automaticity and conduction disturbances in canine ventricular myocardium?
Do depolarizing currents and chlorpromazine induce automaticity and conduction disturbances in canine ventricular myocardium?
The study demonstrates mechanisms of automaticity and conduction delay in canine myocardium, providing insights into early myocardial infarction arrhythmias and phenothiazine-induced fatal ventricular arrhythmias.
Answers are grounded in this paper and cite their sources.
May inform mechanisms of early MI and phenothiazine-related arrhythmias; leaves open translation to human ventricular tissue.
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 an 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, chloropromazine induced time (preceding cycle length)-dependent decrease in conduction velocity within the ventricle. Thus QRS-duration of non-premature beats was lenghtened 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 bue 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.
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Arita et al. (1977) studied this question.
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