Abstract
The distribution of two oxidative enzymes (DPN-diaphorase and succinic dehydrogenase), two hydrolytic enzymes (acid and alkaline phosphatase) and data on mitochondria were described as to their relationship to the histopathology of cerebral arteriosclerosis. Incomplete necrosis of gray matter was characterized by a patchy, irregular decrease of oxidative enzyme activity in the neuropil. Complete necrosis (infarcts) showed a loss of enzyme activity in the tissue except the walls of capillaries which still showed activity of oxidative enzymes and also alkaline phosphatase. Hypertrophic astrocytes in the adjacent tissue were characterized by excessive increase of oxidative enzyme activity. Microglia showed little oxidative enzyme activity but strong activity of acid phosphatase. Fatty degeneration of cells was consistently accompanied by decreased oxidative enzyme activity; there was no such inverse relationship for acid phosphatase. Study of capillarization, normal histochemistry, and of pathological changes of the periarterial tissue suggested that the wall of thick arteries normally provided sufficient nutrition of the periarterial tissue. Impairment of this function in arteriosclerosis was considered responsible for the formation of periarterial scars in arteriosclerosis.
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