Ethanol delays and reverses lysophosphatidylcholine-induced calcium overload in neonatal rat heart cells

Increased lysophosphatidylcholine, (LPC) production by the ischemic heart i s associated with tissue damage. In vitro, LPC produces an increase in cyto solic [Ca2+], usually followed by cell contracture and lysis. Since ethanol reportedly protect cells during ischemia-reperfusion, we wished to determi ne whether ethanol could protect heart cells against LPC-induced Ca2+ overl oad. Newborn rat heart cells in culture were loaded with Fura-2 and [Ca2+]( i) recorded in individual cells. The presence of 22 or 44 mM ethanol increa sed the time required for 10 muM L-palmitoyl-LPC to produce maximal Ca2+ ac cumulation from 8.4 +/-0.4 min (n=47) to 21.1 +/-2.1 min (n=32; P <0.01) an d 23.8 +/-1.8 min (n=10; P <0.01) respectively. The onset of the [Ca2+](i) increase could be reversed partially by the addition of ethanol (44 or 88 m M). After the addition of 22 mM ethanol, the cells retained the Fura-2 thre e times longer than under control conditions. Ethanol (88 mM) decreased the critical micelle concentration of LPC, thus decreasing the LPC monomer con centration in this solution. La3+ also protected the cells against LPC but no further protection was afforded by the addition of ethanol. Our results suggest that ethanol concentrations commonly found in the blood of social d rinkers protect heart cells against the deleterious effect of LPC.