Indomethacin attenuates early postischemic vasogenic edema and cerebral injury.

Inhibition of cyclooxygenase products by IND given during and after temporary MCAO produced a marked reduction in the incidence of early postischemic BBB opening to albumin, despite the presence of reactive hyperemia. This beneficial effect might be due to direct prevention of endothelial cell damage by inhibition of prostaglandin synthesis. Reduction was insignificant in postischemic brain edema: however, the intensity of postischemic neuronal damage was reduced by IND.