Electrophysiologic effects of vinpocetine and vincamine on isolated rabbit papillary muscle in normal‐ and low‐potassium medium

Abstract

AbstractThe electrophysiologic effects of vinpocetine (VP) on the action potential (AP) of the isolated rabbit papillary muscle were compared with those of vincamine (VC) in normal (5.6 mM)‐ and low (2.7 mM)‐potassium concentrations. In 5.6 mM K+ medium, VC (1 and 10 μM) did not affect the resting potential (RP) but increased AP duration at 50% and 90% of repolarization (APD50 and APD90). At 10 μM, a decrease in maximal depolarization velocity (Vmax) was also observed. Under these conditions, VP (1 and 10 μM) hyperpolarized the RP and at 10 μM increased both Vmax and AP amplitude. VP (1 μM) shortened AP duration at 30% of repolarizaton (APD30), but did not significantly modify APD50 and APD90 at 1 and 10 μM. The effects of VP on APD30, APD50, APD90, and Vmax were significantly different from those of VC. Reducing extracellular K+ from 5.6 to 2.7 mM did not significantly modify the effects of VC on AP, except for the RP, which was hyperpolarized. The changes in RP and Vmax caused by VP (1 μM) in low‐K− medium were significantly different from those caused by the compound in normal‐K+ medium were significantly different from those caused by the compound in normal‐K+ medium. However, the decrease in Vmax and increase in APD30, APD50, and APD90 obtained with VC were significantly different from those seen with VP. VC increased AP duration in both normal‐ and low‐K+ concentration. As such, VC poses the risk of “torsades de pointe” dysrhythmia, associated with a long QT interval, even in patients with normal serum K+ levels. On the other hand, our results indicate that such dysrhythmias are not expected with VP even in patients with hypokalemia.