Key result
Combined calcium and potassium channel activators reverse quinidine-induced negative inotropy and shorten refractory periods in vitro.
Why the study?
The modulation of cardiac effects of quinidine by activators of sodium, calcium, and potassium channels was investigated to explore potential treatments for quinidine intoxications.
Do activators of sodium, calcium, and potassium channels modulate the cardiac effects of quinidine in vitro?
Do activators of sodium, calcium, and potassium channels modulate the cardiac effects of quinidine in vitro?
In vitro evidence suggests that a combination of a calcium channel activator and a potassium channel opener might improve the treatment of quinidine intoxication.
May warrant caution against clinical use in quinidine intoxication; leaves open whether channel modulators merit in vivo testing.
Quinidine (25.5 mumol/l) reduced the beating frequency of isolated right guinea-pig atria, caused a negative inotropic effect in papillary muscles and slightly raised the contractile force of left atria. The functional refractory period of both tissues was prolonged. A 20% increase of the extracellular sodium concentration did not reverse the effects of quinidine. The Na-channel activator BDF 9148 (1 mumol/l) and the Ca-channel agonist Bay-K-8644 (0.5 mumol/l) further increased the contractile force and caused an additional prolongation of the functional refractory period in quinidine-pretreated atria. Only Bay-K-8644 was able to reverse the negative inotropic effect of quinidine in papillary muscles. The influence of Bay-K-8644 on the contractile force in quinidine-pretreated muscles was not attenuated by lemacalim (3 mumol/l), an activator of ATP-dependent potassium channels, but the duration of the functional refractory period was significantly reduced. These results suggest that a combination of a calcium channel activator and a potassium channel opener might be able to improve the treatment of quinidine intoxications.
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Helmut Brasch (1995) studied Quinidine intoxication. Sodium, Calcium and Potassium Channel Activators (BDF 9148, Bay-K-8644, lemacalim) vs. Quinidine alone (25.5 mumol/l) was evaluated on Contractile force and functional refractory period. A combination of a calcium channel activator and a potassium channel opener reversed the negative inotropic effect and reduced the prolonged refractory period caused by quinidine in vitro.
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