Experiments in rats showed that in vitro cell membrane transport of Na and K in the liver was severely impaired during hemorrhagic shock. This defect was rapidly corrected in early shock by non specific treatment with volume replacement. As shock continued, the depression of cell membrane transport was not rapidly corrected by treatment and persisted. Other alterations in hepatic cell function produced by shock which were measured were rapidly corrected by treatment. Persistent depression of cell membrane transport may be a limiting factor in severe, prolonged shock.