Leakage, Migration, and Absorption of Autoserum Protein in Experimental Cerebral Edema

Abstract

Evans blue, horseradish peroxidase (HRP), and lanthanum have long been used as tracers in experimental brain edema, but these substances appear to modify in vivo reactions. In this study, to exclude such foreign body reactions, ischemic and traumatic cerebral edema was produced in rats previously inoculated with HRP, and leakage of anti-HRP antibodies from microvessels and their migration into brain tissue, as well as absorption of edema fluid by the ventricular lining were observed. Wistar rats were immunized with four HRP booster shots in four weeks. Ischemic and traumatic cerebral edema were produced by means of transcarotid embolization and cold injury techniques, respectively. Immunohistochemical techniques were used to observe the location of anti-HRP antibodies. Three hours after embolization, no leakage of anti-HRP antibodies from capillaries was observed in the ischemic lesion and surrounding brain tissue. However, 24 hours after embolization, leakage of anti-HRP antibodies from venules and capillaries in the ischemic lesion was clearly detected. Uptake of anti-HRP antibodies by neurons and glial cells was also noted. Anti-HRP antibodies migrated along the nerve fibers in the white matter and reached the subependymal layer of the lateral ventricle. The drainage sites for anti-HRP antibodies were those not protected by the blood-brain barrier, that is, the subfornical region at the root of the choroid plexus of the lateral ventricle, the pineal body at the root of the choroid plexus of the third ventricle, the hypophysis and its vicinity, and the choroid plexus itself. The findings in the cold injury model were similar to those in the ischemic model at 24 hours after embolization.