Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. Scanning and transmission electron microscopy of such pial arterioles showed discrete destructive endothelial lesions the density of which correlated with the degree of vasodilation. Abnormalities of the vascular smooth muscle were seen in all dilated arterioles but affected only a small number of smooth muscle cells. The oxygen consumption of pial arterioles from cats subjected to hypertension was significantly reduced in comparison to that of vessels from normal animals. The arteriolar abnormalities induced by hypertension were inhibited by pretreatment with inhibitors of cyclooxygenase (indomethacin or AHR-5850) or by topical application on the brain surface of scavengers of free oxygen radicals (mannitol or superoxide dismutase). The results suggest that the mechanism of the arteriolar abnormalities from acute hypertension involves a sudden increase in prostaglandin synthesis that leads to generation of free oxygen radicals.

Diffuse loss of cerebellar Purkinje cells and to some extent, of granule cells occurred in a 78-year-old woman who had been continually treated with phenytoin for more than 20 years and in whom progressive cerebellar deficits developed in the later years of life. In the absence of other demonstrable cause, the selective morphologic changes in the cerebellum are attributed to long-term administration of phenytoin.

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We investigated the fine structural details of the presence of apparently newly formed oligodendrocytes within reactive astrocytes in white matter lesions obtained by biopsy from seven cases (3 multiple sclerosis (MS); 3 progressive multifocal leukoencephalopathy (PML); 1 with nonspecific reactive changes next to a sarcoid granuloma). Intact oligodendrocytes were found within astrocytic cytoplasm in two acute MS lesions and also in the reactive white matter lesion. The internalized cells appeared to lie within membrane-bound vacuoles. Formation of rudimentary junctions was observed between the internalized cells and host astrocytes. Sometimes more than one oligodendrocyte was seen in the same astrocyte. Our study suggests that this newly recognized interaction between astrocytes and oligodendrocytes is not restricted to acute MS lesions and probably represents emperipolesis rather than phagocytosis. This apparently nonspecific finding may be expected in any lesion with a proliferation of astrocytes and oligodendrocytes. The precise mechanism of this phenomenon or its functional significance is not entirely clear.

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