The effect of a short period (3-4 hr) of exposure to cold on the liver's circulation and metabolism has been studied in sheep fed 6 hr or 21 hr before experiment.In the cold the animals had a significantly increased heart rate, cardiac output, hepatic portal blood flow, mean arterial blood pressure and pulse pressure. Total peripheral resistance fell in the fasted animals when they were exposed to cold, but not the more recently fed animals. Exposure to cold significantly increased the total body oxygen consumption and oxygen consumption of the liver, but not that of the portal-drained viscera (gut, spleen, pancreas, omental adipose tissue). Recent feeding significantly increased the net rate of release of volatile fatty acids from the portal-drained viscera, and significantly increased their net rate of uptake by the liver. In the recently fed animals, exposure to cold further increased the visceral release, portal plasma concentration, and hepatic uptake of volatile fatty acids. Exposure to cold, and fasting, both significantly increased the circulating (arterial) plasma level of free fatty acids and glycerol, and increased their net rate of uptake by the liver, significantly in cold exposure but not in fasting.The results show that the liver makes a small contribution to the total increase in oxygen consumption in the cold. The liver also has an increased uptake of fatty acids and glycerol during cold exposure.Mammals increase their total body oxygen consumption (V02), and therefore heat production, when they are exposed to cold. It is not known precisely which tissues are responsible for this increase. In particular it is not known to what extent the liver is one of the organs in the body that has an increased heat production during cold exposure. Functional evisceration of anaesthetized cold-acclimated rats, which includes ligation of the portal vein, does not prevent them from increasing their total body VO2 in the cold, by the same amount as control animals. However, this technique does not eliminate the possibility that other tissues may compensate for any loss of liver heat production [Depocas, 1958]. Measurements of the temperature difference between the hepatic vein and the hepatic portal vein in unanaesthetized dogs show an increase in the temperature difference when ice is applied to the skin of the animal [Fedorov and Shur, 1942] suggesting an increase in liver heat production in response to a cold stimulus. Similar measurements of liver temperature, corrected for liver blood flow (Q), show a fall in liver heat production when unanaesthetized rats, acclimated to 20°C, are put into a warmer environment [Stoner, 1973].The present experiments were designed to measure the V02 of the liver and relate this to total body V02 during acute cold exposure of unanaesthetized sheep. In view of the reported changes in lipid oxidation in sheep during cold exposure [Graham, Wainman, Blaxter and Armstrong, 1959] and the increase in circulating free fatty acids (FFA) [Bost and Dorleac, 1965] and glycerol 107