Histochemical examinations of the cerebral cortex of rats were performed using the Falck-Hillarp method, to observe an enzymatic blood-brain barrier mechanism of intracerebral capillary endothelium and a repairmechanism of damaged blood-brain barrier with glucocorticoids. After depletion of the endogenous monoamines with a large dose of reserpine, dopamine and trypan blue were given intraperitoneally to the three groups of rats; control group, cold injury group, and cold injury group treated with dexamethazone. In the control group, dopamine and trypan blue remained in the capillary lumen and had no penetration into the cerebral parenchyma. In the cold injury group, dopamine and trypan blue penetrated into cerebral parenchyma freely through the endothelium in the edematous regions. Dopamine was uptaken into neurons and astrocytes, and trypan blue penetrated into neuropil in the edematous regions. In the cold injury group treated with dexamethazone, dopamine was uptaken into the capillary endothelium in the edematous regions. Trypan blue was not found in the capillary endothelium. From these findings, it is concluded that the capillary endothelium loses an enzymatic barrier mechanism by the cold injury, but that dexamethazone restores the protective function of the capillary endothelium to dopaminepenetration into the cerebral parenchyma. It is suggested that dexamethazone activates an enzymatic reaction in the endothelium or produces a structural repair of the endothelial basement menbranes and astrocytic feet.