Cation transport capability was measured in liver slices of rats bled to mean arterial blood pressure of 40 mm Hg. This pressure was maintained for: 1/2 hr without return of any shed blood (early shock); 1 hr with slow return of 30% of shed blood (intermediate shock); or 2 hr with slow return of 70% of shed blood (late shock). In vitro sodium potassium transport was inhibited in early, intermediate, and late shock. This was accompanied by a loss of cell volume regulation. Sodium and water contents increased and tissue adenosine nucleotides (ATP, ADP, and AMP) decreased with shock. The decreases in ATP, ATP:ADP ratio, and the energy charge values in intermediate and in late shock probably were not of such a magnitude to indicate complete loss of the in vitro sodium potassium transport. The impairment of cation transport with shock could thus be related to factor (or factors) other than energy availability. The in vitro cation transport was restored to normal with reinfusion of all shed blood and Ringer's lactate in early shock. This did not occur in intermediate shock. Alterations in sodium potassium transport would severely impair the capability of the cells to extrude water, which would lead to cell swelling. This in turn could contribute to critical loss of interstitial and vascular fluids resulting in decreases in the effective circulatory volume in shock.