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In order to investigate the expression of endothelin-like immunoreactivity in astrocytes of viral infections of the human brain the avidin-biotin peroxidase complex method and a polyclonal antiserum were used. Autopsy material was obtained from 5 cases of herpes simplex encephalitis, two of progressive multifocal leukoencephalopathy (PML) and two of subacute sclerosing panencephalitis (SSPE). All the 5 herpes simplex encephalitis cases presented groups of immunoreactive astrocytes around necrotic, inflammatory lesions. The PML cases exhibited a large number of immunoreactive astrocytes in and around lesions of the white matter. The cases of SSPE disclosed numerous, markedly stained fibrillary immunoreactive astrocytes; they were most abundant in degenerated regions of the white matter. The processes and peripheral cytoplasm of giant astrocytes in the PML cases contained immunoreactive material but the perinuclear region was devoid of such material. In the herpes simplex and the SSPE cases immunoreactivity was present throughout the cytoplasm and processes of reactive fibrillary astrocytes. Many nerve cells in the cerebral cortex, hippocampus, cerebellum and pons of control cases exhibited endothelin-like immunoreactivity but this occurred in only exceptional astrocytes of control cases. Endothelin-like immunoreactivity was not present in the oligodendrocytes and vascular endothelial cells of controls and cases of virus infection. The expression of endothelin-like immunoreactivity in astrocytes in human viral diseases reflects probably an increased intracellular content of endothelin. If this peptide is released from such astrocytes, it may act as a mitogen and by inducing constriction of arterioles it may influence the microcirculation.

The avidin-biotin peroxidase complex method and a polyclonal antiserum were used to investigate the distribution of endothelin-1-like immunoreactivity of cerebral astrocytes in autopsy cases of Alzheimer's disease compared with controls. The cases of Alzheimer's disease presented numerous astrocytes with intense endothelin-1-like immunoreactivity of the cell body often extending into the finest ramifications of the cell processes. Absorption of the antiserum by the corresponding antigen eliminated this immunostaining. The immunoreactive astrocytes were most consistently present in the subcortical white matter of the cerebral hemispheres and the folia of the cerebellum. The immunoreactive cells were often located in small clusters close to blood vessels. Five of the seven cases showed immunoreactive astrocytes in the molecular layer of the cerebral cortex and three of the seven cases presented regions in which immunoreactive astrocytes appeared to be located in the periphery of plaques. The pons contained small groups of immunoreactive astrocytes in five of the cases. The cerebellum had such cells in six of the seven investigated patients. Immunoreactive astrocytes were very rare in control cases without cerebral disease. Many nerve cells in the cerebral neocortex, hippocampus, cerebellum and pons of Alzheimer cases and controls exhibited endothelin-1-like immunoreactivity. Oligodendrocytes and endothelial cells of blood vessels of controls and Alzheimer cases did not show such immunoreactivity. The expression of endothelin-1-like immunoreactivity in astrocytes of Alzheimer's disease probably reflects an increased content of endothelin-1. If endothelin-1 is released from such astrocytes it may reach smooth muscle cells of the intracerebral blood vessels and disturb micro-circulation since this compound is a most powerful vasoconstrictor peptide.