The integrity of the blood-brain barrier was studied in a new model of closed head injury, and in an established model of fluid percussion injury, in the rat. Brain injury in this new model is induced by impact and acceleration of the protected rat skull. Severe hypertension is not a characteristic of this new model as compared to the tremendous surge following direct dural percussion. This is important because of the well known sensitivity of the cerebral microvasculature for acute hypertension. Using a radioactive tracer technique the dysfunction of the barrier was quantified. It is shown that the BBB is temporarily damaged due to trauma, subsequent arterial pressure surge, as seen in the percussed animals, deteriorates the dysfunction of the barrier even further. This study indicates that vascular damage is a key event following head injury. Yet the concomitant basic pathophysiological sequelae of different models must be considered when studying barrier damage and cerebral edema following brain injury. Time window studies of the barrier indicate that the barrier seals within a few hours following severe concussive head injury, and in the absence of a hypertensive surge.