Effects of diltiazem on action potentials of atrioventricular node and bundle of His cells in rabbit heart
Abstract
By microelectrode techniques, the electrophysiological effects of the calcium channel blocking agent diltiazem on isolated rabbit AV node and His bundle preparations were studied. Diltiazem (0.28 to 1.12 micromol/L) had no effect on APA and Vmax of upper AV nodal cells (AN). The drug caused a dose-dependent increase in stimulation threshold as well as corrected AVN recovery time and AVN spontaneous rate decreased. ERP of AN cell was significantly prolonged by diltiazem without any change in APD95 exhibiting obvious post-repolarization regractoriness.
Nodal-His (NH) cells were more sensitive to diltiazem than AN cells. Vmax was decreased, APD50 and APD95 were shortened, ERP and A-H conduction time were lengthened by diltiazem, while APA remained the same as control. After the action of 1.12 micromol/L diltiazem, the prolonged ERP was greater than that of APD95, also exhibiting post-repolarization refractoriness.
In 3 preparations, the rapid automatic discharges of AP were induced by adequate premature stimulus, thus providing the basis for AVN reentrant tachymardia. After perfusion of 1.12 micromol/L diltiazem, the rapid automatic discharges were all suppressed for the prolongation of conductance and refractoriness in AVN and NH cells, diminished the heterogeneous conductivity and interrupted reentrant circus excitation within this area.
Keywords:
Nodal-His (NH) cells were more sensitive to diltiazem than AN cells. Vmax was decreased, APD50 and APD95 were shortened, ERP and A-H conduction time were lengthened by diltiazem, while APA remained the same as control. After the action of 1.12 micromol/L diltiazem, the prolonged ERP was greater than that of APD95, also exhibiting post-repolarization refractoriness.
In 3 preparations, the rapid automatic discharges of AP were induced by adequate premature stimulus, thus providing the basis for AVN reentrant tachymardia. After perfusion of 1.12 micromol/L diltiazem, the rapid automatic discharges were all suppressed for the prolongation of conductance and refractoriness in AVN and NH cells, diminished the heterogeneous conductivity and interrupted reentrant circus excitation within this area.