Regional distribution of action potential abnormalities induced by subacute right ventricular pressure overload

Right ventricular pressure overload of 3 days' duration was established in cats by banding of the pulmonary artery. To characterize the regional distribution of the resulting electrophysiologic changes, the right ventricular free wall, adjacent pulmonary outflow tract and septum were mounted in tissue bath and examined by conventional microelectrode techniques. Abnormal action potentials, identified by a negative shift of the voltage level of phase 2 with a corresponding accentuation of phase 1, were recorded from sites contiguous to the tricuspid valve and pulmonary outflow tract and in limited adjacent areas. No abnormal action potentials were recorded on the septal surface, apical end of the free wall, or at any right ventricular location in normal or sham-operated cats. Abnormal potentials could be recorded from sites sampled 5 cell layers deep in the endocardium. The number and extent of distribution of cells demonstrating altered action potentials correlated best with increased right ventricular wet weight at time of sacrifice. Abnormal cells responded to epinephrine or elevated extracellular calcium by a shift in plateau voltage towards zero and by an increase in action potential duration prior to usual plateau shortening. Responsiveness of these cells to agents which influence slow inward current suggests pressure overload-induced changes in the cell membrane that limit or otherwise affect availability of calcium. Regional distribution of plateau potential abnormalities may reflect differential physical stress within the myocardium provoked by sudden pressure overload.