EXPERIMENTAL PERITUMOROUS EDEMA - MORPHOLOGICAL AND PATHOPHYSIOLOGICAL OBSERVATIONS

In 23 cats, vasogenic brain edema was produced by stereotaxic xenotransplantation of the glial cell clone RG 2 into the internal capsula of the brain. The resulting tumor grew to a diameter of 0.5-1 cm within 2-3 weeks; thereafter it was either rejected, or the animal died. One to 4 weeks after the implantation, the EEG, intracranial pressure, and blood flow were recorded using labelled microspheres. The permeability of the blood-brain barrier was tested with Evans blue, and the animal was subsequently killed by air embolism. Tissue samples were taken from peritumorous and contralateral white and grey matter, and assessed for water and electrolyte content, and blood flow. Adjacent sections were fixed in formalin and investigated for permeability disturbances of the blood-brain barrier, and for the spread of peritumorous edema by tracing intracerebral serum albumins with a specific immunofluorescent technique. Permeability disturbances of the blood-brain barrier were restricted to the tumor, but there was, after 2 weeks, massive leakage of serum albumins into the surrounding white matter. Water content in the peritumorous white matter increased from 69.1±0.9 to more than 80%, reaching a maximum after 2-3 weeks. Sodium content rose from 163 to 390 meq/kg d.w., whereas potassium remained almost constant. Blood flow in the edematous white matter was markedly reduced from 32.2±5.6 to 16.5±1.4 ml/100 g/min after 4 weeks. The decrease was due to the expansion of tissue volume and not to an increase in vascular resistance. Fourier transform of the EEG revealed a significant slowing of the mean frequency on the affected side in 6 out of 13 animals. There was no consistent correlation with either the duration of survival, the water content, electrolyte shifts, blood flow or intracranial pressure. EEG changes, in consequence, seem to result from direct influence of the tumor on brain parenchyma, rather than from peritumorus edema or intracranial hypertension. © 1979 Springer-Verlag.