Vascular permeability to horseradish peroxidase in brainstem lesions of thiamine-deficient rats.

In the early brainstem lesions of acute dietary thiamine deficiency in rats, an outstanding feature is the occurrence of edema. This study, using horseradish peroxidase as a marker, confirms and extends our previous observations using fluorescent dye-labeled albumin that vascular permeability to proteins remains essentially intact during this phase, and becomes altered only when necrosis and hemorrhage supervene. In addition, however, although a minor degree of pinocytotic transendothelial transport and pericytic uptake of horseradish peroxidase was found in both normal animals and in the early lesions, in the late lesions there was markedly enhanced pinocytotic transport but no evidence that interendothelial junctions were disrupted. Reaction product was present in the vascular basement membrane regions and in the extracellular spaces of the neuropil, as in other forms of reactive edema. The localized cerebral edema in thiamine deficiency lesions is thus a biphasic phenomenon. It occurs initially in the absence of vascular permeability change and perhaps as the result of defective active transport related to the deficiency state. In contrast, the late edema is the result of gross breakdown of barrier function to protein, with enhanced pinocytotic transport and extracellular accumulation of the marker in the neuropil.