Abstract
The process of the progression and resolution of vasogenic brain edema was evaluated in a rat cold injury model by using magnetic resonance imaging (MRI), immunohistochemical staining and measurement of water content (dry weight method). As we reported previously, extravasated protein migrated from the cold-injured lesion not only to the ipsilateral white matter but also into the contralateral hemisphere through the corpus callosum, a process which we designated as “routed protein migration”. Twenty-four to forty-eight hours after cold injury, extravasated proteins had spread to adjacent areas, and 3-4 days after the injury, they disappeared gradually from the areas remote from the lesion. In the electronmicroscopic study, horseradish peroxidase-reactive substances were observed in the extracellular spaces of nerve fibers, the basement membrane of vessels, intercellular spaces between ependymal cells, and so on. These observations suggested that extravasated protein was cleared into the blood stream, and also probably into the cerebrospinal fluid through the intercellular space between ependymal cells.
MRI findings showed a high signal intensity around the cold injury, and this high signal intensity spread gradually to the ipsilateral and contralateral hemispheres. These findings were almost parallel to the movement of extravasated protein.
Water content of the injured hemisphere was significantly increased immediately after cold injury, but the increment of water content of the contralateral hemisphere was minimal. The increase of water content is consistent with the MRI evidence of the existence of edema in both hemispheres. These observations suggested that the movement of extravasated protein and edema fluid was almost parallel, and vasogenic brain edema extended to a wide area of the brain through the white matter, followed by reabsorption into the blood stream, and clearance to the cerebro-spinal fluid through the intercellular spaces between ependymal cells.
