Ischemic brain edema : Morphological aspects in its formation, movement and resorption

Abstract

The underlying mechanisms that lead to brain edema following ischemic insult have been subject to much debate.
In the first study, experimental cerebral infarction was produced in 25 dogs by injecting 1 or 2 silicon rubber cylinders through the cervical internal carotid artery. The animals were sacrificed 24 hours after embolization. Freezefracture studies were conducted on the plasma membrane of the capillary endothelium from 15 control and 25 ischemic dogs. No definite findings of tight junction opening were made in the ischemic preparations. Pinocytotic vesicles were seen as concave area on the protoplasmic face (PF) of the plasma membrane and as protrusions on the exoplasmic face (EF). The average pinocytotic vesicle count per square micron was increased in ischemic animals. On the luminal side, it reached 22.0 ± 1.2 sq μ in the 50 PF samples and 29.5 ± 1.31 sq p in the 50 EF samples in the experimental preparations, as compared to 7.2± 0.5 sq μ in the 50 PF samples and 9.0 ± 0.6 sq μ in the 50 EF samples in normal cortex. The average area of the vesicles was also enlarged in experimental animals : 4, 990 ± 798 sq nm in the 50 PF samples and 4, 762± 878 sq nm in the 50 EF samples, as compared to 3, 765 ± 570 sq nm in the 50 PF samples and 3, 404 ± 573 sq nm in the 50 EF samples in normal cortex (p>0.01). These results indicate that transcellular transportation by pinocytotic vesicles plays an important role in the increase of capillary permeability observed in an ischemic model.
In the second study, ischemic cerebral edema was produced in 10 rats by means of transcarotid embolization which have been previously immunized by horseradish perioxidase (HRP). The animals were sacrificed 24 hours after embolization. Immnuohistochemical technique was used to observe the location of anti HRP antibodies. Leakage of anti-HRP antibodies from venules and capillaries in the ischemic lesion was clearly observed. Uptakes of anti-HRP antibodies in the neurons and glial cells were also observed. Anti-HRP anti-boddies migrated along the nerve fibers in the white matter and reached the subependymal layer of the lateral ventricle. The drainage sites of anti-HRP antibodies in the brain were the site being devoid of the blood-brain barrier, that is, the subfornical organ at the root of the choroid plexus of lateral ventricle, the pineal body at the root of the choroid plexus of third ventricle, also the hypophysis and its vicinity, and the choroid plexus itself.