Ethanol suppresses smooth muscle cell proliferation in the postprandial state: a new antiatherosclerotic mechanism of ethanol?

Epidemiologic studies suggest that moderate amounts of ethanol may reduce cardiovascular risk. The mechanisms of the alcohol-associated risk reduction are not known exactly. Vascular smooth muscle cell proliferation represents an important phenomenon in the pathogenesis of atherosclerosis. Recently, it was suggested that metabolic changes during the postprandial phase may be important in the pathogenesis of atherosclerosis. Therefore, we evaluated the effect of postprandial plasma with and without ethanol on the proliferation of rat vascular smooth muscle cells. Identical meals containing 1 g fat/kg body wt were given with and without ethanol (38 +/- 0.5 g) to eight healthy young men. Blood was drawn hourly during an 8-h postprandial period; the plasma was separated and added to the cell cultures (0.3%, by vol). The proliferative response (DNA synthesis) of these cells was assessed by measuring the incorporation of [methyl-3H]thymidine. The maximal blood ethanol concentration of 11.5 +/- 0.6 mmol/L (mean +/- SEM) was attained within the first hour. The ingestion of the meal with ethanol led to a 20% reduction in the capacity of postprandial plasma to induce thymidine incorporation into smooth muscle cells compared with the meal without ethanol (P < 0.05). These results suggest that ethanol may reduce cardiovascular risk by modulating vascular muscle cell growth during the postprandial period. Considering the amount of time humans spend in the postprandial state during their lifetimes, these findings may be of great importance in the pathogenesis of atherosclerosis.