Studies on slow cardiac action potentials occurring in potassium-rich media as a simulation of the early phase of myocardial infarction. Influence of potassium-conductance blockers and antiarrhythmic drugs.

In the acute phase of myocardial infarction, a marked intracellular potassium loss and the lack of intact coronary circulation are known to result in extracellular hyperpotassemia partially depolarizing the damaged cells. To simulate these conditions, isolated guinea pig papillary muscles were superfused with K+-rich Tyrode solution, the minimal norepinephrine concentration required to trigger slow action potentials (SR) was measured, and the characteristics of SR were studied with glass microelectrodes. The threshold norepinephrine concentration was found to be about 1.04 x 10(-6)M. This threshold concentration was decreased by substances inhibiting the outward potassium currents (4-aminopyridine, tetraethylammonium, cesium); the SR duration and the maximal rate of depolarization were increased by them. Lidocaine and procainamide have no influence on these parameters. Phenytoin and the Mg2+ ion were found to have a marked inhibitor effect by increasing the threshold norepinephrine concentration and decreasing the maximal rate of depolarization of SR.