[Effects of low-frequency pulsing magnetic field upon the respiratory metabolism and transmembrane ion fluxes of perfused rat livers].

UNLABELLED

Influence of magnetic fields on biological systems is not completely clear. Recently, experiments on the effects of weak not heat inducing electromagnetic fields concerning biological systems have been reported. We have investigated the effects of the weak low-frequency pulsing magnetic field (PMF) concerning the respiratory metabolism and transmembrane ion flux of perfused rat livers.

MATERIALS AND METHODS

Livers from male Wistar rats were perfused via the portal vein with 95% O2-5% CO2 saturated Krebs-Henseleit Bicarbonate Buffer maintained at 32 degrees C. In 48 hrs fasted rats, lactate was administered in the perfusate as a substrate of gluconeogenesis in case of necessity. PMF generated by the solenoid coil was applied to the perfused livers. For monitoring of respiratory metabolism of the perfused livers, scanning spectrophotometry and NADH fluorometry were applied to the surface of the liver. The effluent was monitored for PO2 and analyzed for glucose, lactate and pyruvate. Ca2+, Mg2+, Na+, K+, Cl- ion from effluent were also analyzed.

RESULTS

By being exposed to a low-frequency PMF, the O2 consumption increased in the perfused livers of the fed rats, but the degree was variable according to the metabolic state of the liver of each rat. In order to bring about a maximum reductive state, ethanol was given to the perfusate. Ethanol caused an increase in NADH and Lactate/Pyruvate ratio and O2 consumption and an inhibition of glucose production. By exposure to PMF the metabolism of perfused liver was shifted to the re-oxidative state. In lactate administered perfused liver of the 48 hrs fasted rats, PMF caused an increase in the livers sensitivity to glucagon. As regards the transmembrane ion fluxes, PMF acted antagonistically to the ethanol effect, especially when we used perfusate with low Ca2+ concentrations. So that an intimate association between PMF and intracellular Ca2+ regulating system was suggested.