Neovascularization with blood-brain barrier breakdown in delayed neuronal death

Various kinds of acute pathological events in the central nervous system, s uch as ischemia, hemorrhage, and trauma, often cause brain edema. The edema may advance for days or weeks while inducing extensive damage in neural fu nction, regardless of the extent of the original damage, and often results in death. Delayed edema is thought to be vasogenic; how ever, the mechanism underlying edema induction remains unknown. We found delayed vascular cell proliferation with a blood-brain barrier breakdown in and around the gerbi l CA1 hippocampus, a region known to be involved in delayed apoptotic neuro nal death 2-6 days after transient ischemia. Vascular cell proliferation, a ssessed by SH-thymidine incorporation, was most prominent 4-6 days after is chemia, and extravasation of exogenously applied dye or endogenous serum al bumin from blood vessel was observed concomitantly. We propose neovasculari zation in delayed neuronal death as a cause of brain edema advancing days a fter neurological events, (C) 2000 Academic Press.