[Inotropic, cardioprotective and antiarrhythmic effects of ginseng preparations]

The review systematizes data on the cardiotropic effects of ginsenosides studied in vivo and in vitro. It has been shown that ginsenosides decrease the heart rate both in vivo and in vitro. It is established that triterpenoid saponins inhibit contractility of isolated heart and atrium and exhibit negative inotropic effect in the experiments with isolated cardiomyocytes. Ginsenosides shorten duration of the action potential and decrease the amplitude of slow action potential in cardiac cells. There is evidence that ginsenosides inhibit Ca2+ channels. Triterpenoid saponins of ginseng improve the cardiac tolerance to ischemic and reperfusive damage both in vivo and in vitro. These saponins increase cardiac resistance to the toxic action of isoproterenol and adriamycin. Triterpenoid saponins enhance the tolerance of cardiomyocytes to oxidative stress in vitro. Ginsenosides prevent the appearance of ischemic/reperfusive arrhythmias and decrease the incidence of arrhythmias induced by epinephrine. The molecular mechanisms of action of triterpenoid saponins is discussed and their interactions with steroidal hormone receptors, protein kinases, NO synthase, K(ATP) channels, and Ca2+ channels are considered.