Morphological and chemical studies in cerebral edema: Triethyl tin-induced edema

Abstract

Edema of the brain was produced in rats by chronic oral administration of triethyl tin hydroxide. This resulted in swelling and increased water content of the central nervous system. The edema was essentially restricted to the white matter, although some changes of varying degree were also observed in the gray matter, particularly in the basal ganglia and in the geniculate bodies. The edema is reversible and severely afflicted rats recovered from the neurological symptoms upon cessation of triethyl tin feeding. The edematous brain did not stain vitally with trypan blue. The blood-brain barrier remained essentially impermeable to 131I-labeled serum albumin. The rate of uptake and radioautographic distribution of 14C-labeled glycine was identical in normal and edematous white matter. The sodium and chloride content increased and potassium decreased in the edematous brain. The diminished potassium concentration was merely the result of dilution of cerebral potassium by edema fluid of low potassium content. However, sodium chloride was markedly increased even when calculated on a dry weight basis. The exchange rate of 24Na between plasma and edematous brain was reduced. The uptake of 42K revealed no significant difference between the brains of normal rats and those treated by triethyl tin. Experiments with 32P were not conclusive but a possibly significant difference in the pattern of deposition of this isotope was observed in edematous brains. The results indicate that the edema fluid in triethyl tin poisoning is a plasma filtrate that differs from the fluid of cold induced cerebral edema and edema produced by hypercapnic hypoxia.