ETHANOL PROMOTES RAPID DEPLETION OF INTRACELLULAR FREE MG IN CEREBRAL VASCULAR SMOOTH-MUSCLE CELLS - POSSIBLE RELATION TO ALCOHOL-INDUCED BEHAVIORAL AND STROKE-LIKE EFFECTS

The acute effects of ethanol on intracellular free magnesium ions ([Mg2+](i)) in cultured canine cerebral vascular smooth muscle cells (VSMCs) were studied by digital imaging microscopy using the Mg2+ fluorescent probe mag-fura-2. In 0 mM ethanol, the basal level of [Mg2+](i) was between 500-700 mu M with a heterogeneous distribution within the cells; [Mg2+](i) was greater in the perinuclear than in the peripheral region. Treatment of the cells with 10, 25, and 100 mM ethanol resulted in rapid (within 30 s) concentration-dependent reduction in [Mg2+](i); the greater the concentration and the greater the duration of acute exposure, the greater the fall in [Mg2+](i). Exposure of cerebral VSMCs to 100 mM ethanol resulted in a 57% reduction in [Mg2+](i) (i.e., from 510 +/- 40 to 220 +/- 30 mu M). These observations are consistent with the tenet that ''binge drinking'' of ethanol could result in cerebrovasospasm, ischemia, and rupture of cerebral blood vessels as a consequence of depletion of cerebral VSMC [Mg2+](i). Deficits in [Mg2+](i), O-2, and nutrient delivery could account in part for some of the behavioral actions of alcohol.