Weak Magnetic Field at 16 Hz Affects Cardiac Myocyte Ca2+ Transients and Reduces Cells Damage Caused by Hypoxia

Abstract

Effects of extremely low intensity and frequencies of Weak Electromagnetic Fields (WMF) on the cardiovascular system have been reported. However, little is known about the physical mechanism of interactions between magnetic fields and physiology. The aim of this study was to explore the effect of WMF at Extremely Low Frequencies (ELF) on Ca 2+ transients, and to investigate the influence of magnetic field following hypoxic stress, in cardiac cell cultures. Indo-1 loaded cells, which exposed to WMF at 16 Hz, demonstrated a faster reduction in cytosolic Ca 2+ transients compared to control cells (75±4% vs. 25±8%). This effect was not observed in other low frequencies. BDM (2,3-butanedione 2-monoxime), which inhibits contraction but not Ca 2+ transient, did not inhibit the effect of WMF on the reduction of Ca 2+ transients at 16 Hz, suggesting that the effect probably involves ion regulation. However, treatment with the K ATP channel blocker, glibenclamide, followed by 16 Hz exposure, blocked the reduction in cytosolic Ca 2+ transients, while treatment with chromanol 293B, a selective blocker of the delayed rectifier K + current channels (I ks ), or the potassium channel opener, pinacidil, did not inhibit the effect. In addition, cardiomyocytes exposure to WMF-ELF at 16 Hz 30 min prior to hypoxia, exhibited a significant reduction in lactate dehydrogenate level and low percentages of death cells vs. hypoxic treatment. In conclusion, WMF at low frequency of 16 Hz induced changes in cardiomyocyte contractions by reducing Ca 2+ transients, most probably through activation of K ATP ion channels. Cells subjected to WMF frequency prior to hypoxic stress, exhibited significantly reduced cardiomyocytes damage.