title: Structural and vasoactive factors influencing intracerebral arterioles in cases of vascular dementia and other cerebrovascular disease: a review. Immunohistochemical studies on expression of collagens, basal lamina components and endothelin-1.
abstract: 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.
authors.affiliation: Laboratory of Neuropathology, Institute of Pathology, University Hospital, Uppsala, Sweden.
authors.forename: W W
authors.initials: WW
authors.lastname: Zhang
authors.forename: T
authors.initials: T
authors.lastname: Badonic
authors.forename: A
authors.initials: A
authors.lastname: Höög
authors.forename: M H
authors.initials: MH
authors.lastname: Jiang
authors.forename: K C
authors.initials: KC
authors.lastname: Ma
authors.forename: J X
authors.initials: JX
authors.lastname: Nie
authors.forename: Y
authors.initials: Y
authors.lastname: Olsson
authors.forename: P
authors.initials: P
authors.lastname: Sourander
mesh_terms: D001160:Arterioles / Q000473:pathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002561:Cerebrovascular Disorders / Q000378:metabolism / Q000473:pathology*; D003094:Collagen / Q000276:immunology / Q000378:metabolism; D015140:Dementia, Vascular / Q000378:metabolism / Q000473:pathology*; D016232:Endothelins / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry
chemical_list: D016232:Endothelins; D003094:Collagen