Histochemistry of the neuroglia and myelin in experimental cerebral oedema

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Abstract
Cerebral edema was induced in rats with injections of vasopressin and feedings of stock rat cubes steeped in a solution of triethyl-tin hydroxide in arachis oil. At the time of sacrifice, the brains were removed and sections were stained by hematoxylin and eosin and metal impregnation methods for cytological study of oligodendrocytes, astrocytes, microglia and neurons. Histochemical methods were used to demonstrate lactic, succinic, glutamic, [alpha]-glycerophosphate (NAD-linked), isocritric (NAD- and NADP-linked), malic and glucose-6-phosphate dehydrogenases; NADH2- and NADPH2-tetrazolium reductases; acid and alkaline phosphatases and uncharacterized Ca++, Na+-activated "adenosine triphosphatase". Some sections were also stained for cytochrome oxidase and lipids. In the animals injected with vaso-pression and water a moderate degree of cerebral edema was seen in 3 out of 9 animals. No morphological changes were seen in the myelin, oligodendroglia, microglia and vessels and no enzymic changes were apparent in the neuroglia or vascular endothelium. In the animals on the diet, all the brains, except one, were visibly swollen grossly. The edema was localized to white matter and adjacent grey matter and appeared to be in or around the myelin sheaths and not primarily within neuroglia. The AT Pase activity decreased in these brains and electron-histochemical study has shown that the loss is mainly from sites on astroglial plasma membranes. No demyelination occurred in these brains. The absence of demyelination in the intoxication in spite of the severe distortion and swelling of white matter, is strong evidence against a pathogenic role of edema in the demyelinating pro-cess. The induced edema within or around the myelin appeared to be ineffective in producing either physical disintegration or chemical degradation of myelin.