1. The effects of physostigmine (70 micrograms kg-1, intravenously) on acid-base status in arterial and venous blood were studied in anaesthetized rabbits subjected to hemorrhagic hypovolemia. 2. Hemorrhagic shock was produced using intermittent bleeding of 50% of the estimated blood volume, during 30 min. Experimental group was treated with physostigmine (70 micrograms kg-1 body mass, intravenously) and the control group with the same volume (0.1 ml) of saline, immediately after bleeding. Blood samples were taken before and after bleeding (0, 15 and 60 min). 3. It was found that physostigmine increased the mean arterial blood pressure, did not change the heart rate, and improved survival of the animals. 4. These effects of physostigmine were associated with significant decrease in venous pH, produced mainly by increased PCO2. This can partly be explained in terms of additional vasoconstriction due to physostigmine action. 5. In arterial blood decreased pH, decreased standard bicarbonate, negative values of excess base and decreased PCO2 were observed both in physostigmine-treated and the control group of animals, indicating partly respiratory compensated metabolic acidosis. These findings indicate that the hypertensive effect of physostigmine in shock was not accompanied by more severe disturbance in arterial acid-base status than was observed in hypovolemic shock alone.