Following hemorrhage, lost blood volume is replaced in two stages. The first stage involves sympathetic nervous system reflex precapillary constriction which results in the shift of interstitial fluid into capillaries. In the second stage, lost blood volume is replaced by the development of hyperosmolality which also results in the movement of interstitial fluid into the vascular compartment. One major component of the hyperosmolality is hyperglycemia which is the result of glycogenolysis in the liver. This glycogenolysis may also be under the control of the sympathetic nervous system. Using a technique of intraportal injection of 6-OH Dopamine in the dog, we have documented the ability to produce selective hepatic sympathectomy. Animals have been examined histologically and physiologically to confirm the technique. We are now able to compare the hypersomolality and hyperglycemia produced by 10% and 30% hemorrhage in fed and fasted animals with normal and sympathectomized hepatic innervation. We are now in the process of distinguishing the effect of sympathetic nervous system and endogenous catecholamine on the control of hyperglycemia after hemorrhage.