A solution of mannitol or urea was infused into the carotid artery of rats to open the blood-brain barrier (BBB) and to find out if such a procedure results in brain injury. Paraformaldehyde-fixed, paraffin-embedded material was available to determine the localization and extent of albumin extravasation by immunochemistry. Other light microscopic and immunocytochemical techniques were applied on consecutive sections to find out if structural damage had occurred. The cerebral cortex, the hippocampus and the basal ganglia of the infused brain hemisphere contained within regions of albumin extravasation scattered, collapsed, acidophilic neurons. In addition, there were multifocal lesions with marked sponginess of the neuropil which contained numerous shrunken, acidophilic neurons and a perifocal astrocytic gliosis. A moderate macrophage infiltration was present in rats with 72 h survival. In conclusion, infusion of hypertonic mannitol or urea into the carotid artery of the rat may result in structural brain damage within regions showing BBB injury. The presence of acidophilic neurons and the macrophage response indicate that some of the brain changes are irreversible.

Albumins↗

PubMedDate not supplied

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.

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.

Arterioles↗