Arachidonic acid release from tissue membranes and/or formation of free radical species have been thought to affect the blood brain barrier permeability and formation of brain edema. To determine whether exogenous arachidonic acid or H202 may alter blood brain barrier permeability, we examined their effect on cultured endothelium derived from cerebral microvessels of human and animals. Release of 51Cr from labeled endothelium exposed to these substance was used as a main marker for the assessment of endothelial injury. The results of these studies indicate that the endothelial cells are susceptible to exogenous arachidonic acid or H202 insult irrespective of their origin. However, human endothelial cells are less affected than animal endothelial cells by the H202-generated system. The findings suggest that a disturbance of the existing balance between the endogenous antioxidant properties of endothelial cells and exogenous oxidant leads to EC injury.
