The relation between the degree of spinal cord compression and the extent of early posttraumatic reaction of astrocytes was investigated in rats using the blocking-weight technique to induce a spinal cord compression at the level of the Th8-9. Immunohistochemistry was used to detect changes in the expression of glial fibrillary acidic protein (GFAP) and vimentin up to 24 h after injury. A mild compression, which did not cause any measurable neurological deterioration, induced a mild increase of GFAP immunoreactivity at 4 h and a more marked and widespread immunoreactivity at 24 h. The greatest increase of GFAP immunoreactive astrocytes occurred in rats with moderate compression of the cord causing reversible paraparesis and in animals with severe compression leading to paraplegia. The increase of GFAP immunoreactivity was present already 4 h after injury in virtually all the segments investigated (Th5-6-Th11-12) and was most marked at 24 h. Vimentin immunoreactivity of control rats was present in the ependymal cells of the central canal, the leptomeninges, and walls of a few intramedullary vessels. Occasional astrocytes were stained. In rats surviving 24 h after moderate and severe compression vimentin immunoreactivity was increased in the walls of intramedullary blood vessels including capillaries of one rostral and one caudal segment. Many macrophages with immunoreactivity appeared and occasional glial cells with astrocyte shape were stained. This investigation shows that within 24 h after compression of the spinal cord a widespread astrocyte reaction occurs. Even a mild compression that does not produce any signs of motor dysfunction can induce widespread astrocyte alterations in the spinal cord. This astrocyte response is more marked in rats with more severe compression leading to more pronounced neurological deterioration. The increase in vimentin immunoreactivity of blood vessels is more localized and occurs in moderate and severe compression of the cord.
The condition of the brain parenchyma in cases of vascular dementia and other cerebrovascular conditions may be influenced by structural and functional changes of the terminal intracerebral blood vessels. Arterioles can develop obliterative lesions, capillaries and postcapillary venules can be altered, causing edema. The first part of this review is focused on expression of different types of collagens and other components of the extracellular matrix in intracerebral arterioles. The changes present in hereditary multi-infarct disease of the brain are compared with those occurring in the Binswanger type of encephalopathy and cases presenting hyalinosis of intracerebral vessels. Deposition of collagens in degenerated parts of the media and adventitia of the arterioles may contribute to impaired blood flow regulation in the brain parenchyma. Fibrillary collagens and basal laminae are probably the most important components of the hyaline material in vessels showing ‘hyalinosis’. The second part of our review concerns the possibility that the vasoactive peptide, endothelin-1, released from reactive astrocytes, can influence the function of intracerebral arterioles. Normal astrocytes do not show endothelin-1-like immunoreactivity, but in cases of infarcts, lacunes, hereditary multi-infarct disease, Binswanger''s encephalopathy and Alzheimer''s disease numerous reactive astrocytes express such immunoreactivity. If endothelin-1 is produced and released from reactive astrocytes it may reach intracerebral arterioles and induce long-lasting vasoconstriction. Endothelin-1 is the most powerful vasoconstrictor peptide known to date and has mitogenic capacity. It may promote cellular mechanisms leading to astrocytic gliosis and neovascularization.
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