Lack of relation between the ventricular refractory period prolongation by amiodarone and the thyroid state in rats.

We investigated the possibility that the prolongation of the ventricular effective refractory period (VERP) by amiodarone might be mediated, at least in part, by inhibition of thyroid influence on the heart. VERP values were measured in vitro in isolated septal preparations obtained from control, thyroidectomized and thyroxine (tetraiodothyronine; T4)- or triiodothyronine (T3)-treated rats. Differences in thyroid influence on the heart between these groups were assessed by changes in the myosin isozyme (V1, V2, V3) pattern. VERP measurements were also done in similar groups treated with amiodarone for 7 days (50 mg/kg/day i.p.). VERP tended to be increased by thyroidectomy and was significantly reduced by T4 or T3 treatment when compared with the control group. Amiodarone treatment significantly prolonged VERP in control (33.4 +/- 1.9 to 45.0 +/- 4.5 msec), thyroidectomized (39.9 +/- 1.7 to 48.3 +/- 2.8 msec), T4-treated (26.2 +/- 1.0 to 37.4 +/- 1.3 msec) and T3-treated rats (25.6 +/- 1.1 to 34.3 +/- 1.3 msec). However, the magnitudes of the VERP prolongation by amiodarone were not significantly different among the four groups. The action of amiodarone on action potential duration was similar to its action on VERP. The myocardial concentrations of amiodarone and desethylamiodarone were not significantly different among the four groups. Amiodarone treatment produced a significant reduction of serum T3 levels in the control and in the T4-treated groups and an increase in reverse T3 levels. Thus, the class III action of amiodarone was not affected, in the present model, by experimental modification of thyroid influence on the heart.