Inhomogeneity of ventricular refractory period in canine heart with quinidine-induced long QT interval: a comparative study on effects of heart rate, isoprenaline, and lignocaine

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Abstract
In anaesthetised open chest dogs, 30 mg·kg−1 of quinidine sulphate was injected intravenously over 5 min to produce QT prolongation. The sinus node was crushed. Effective refractory period (ERP) was determined at eight test points of the right ventricle using extra-stimuli after every seven basic ventricular pacings. Stimuli were of 2 ms duration and 1.5 times diastolic threshold. Temporal dispersion was estimated as the difference between the maximum and the minimum ERP of eight test points. Cycle lengths of basic ventricular drive were 700, 600, 500, and 400 ms. Time course of changes in ERP and its temporal dispersion was tested in five dogs. The effect of a 2 mg·kg−1 bolus injection followed by 70 μg·kg−1·min−1 drip infusion lignocaine, on quinidine-induced changes in ERP was studied in eight dogs, and that of a 0.06 μg·kg−1·min−1 infusion of isoprenaline, was tested in six dogs. ERP was significantly prolonged after quinidine injection (220 ± 20 vs 258 ± 25 ms n = 19, basic cycle length = 500 ms, pvs 33 ± 12 ms n = 19, basic cycle length = 500 ms, pvs 273 ± 16 ms BCL = 500 ms, pvs 23 ± 7, BCL = 500 ms). Isoprenaline significantly shortened both ERP and temporal dispersion (257 ± 27 vs 228 ± 28, pvs 12 ± 4, p<0.01. BCL = 500 ms, respectively). This was also true for ERP and temporal dispersion of the earliest premature depolarisations. Results obtained in the present study might explain the underlying mechanisrn(s) of efficacy of cardiac pacing, lignocaine, and isoprenaline to suppress polymorphous ventricular tachycardia in clinical cases with quinidine-induced long QT interval.