Chronic cerebral hypoperfusion and impaired neuronal function in rats.

Abstract

Background and Purpose Studies in acute cerebral ischemia have shown that reductions in cerebral blood flow of up to 50% do not lead to infarction or alterations in neuronal electric activity. Little is known about the effects of chronic reductions in cerebral blood flow. The purpose of this study was to evaluate neuronal electrophysiological function in brain that had been subjected to a chronic reduction of cerebral blood flow of less than 50%. Based on existing knowledge of thresholds of cerebral ischemia, neuronal electrophysiological function should be unaffected by hypoperfusion of this magnitude.Methods An arteriovenous fistula model in the rat was used to induce chronic cerebral hypoperfusion with reductions of cerebral blood flow of 25% to 50% as measured previously by

Cerebral Hypoperfusion and Delayed Hippocampal Response After Induction of Adult Kaolin Hydrocephalus

“…28 Given that there are differences in the pathology of arteriovenous fistula-and kaolin-induced hydrocephalus, our observations on the neuronal response in the long-term stage of kaolin hydrocephalus strongly resembles the findings of arteriovenous fistula-induced ischemia. 27,28 We postulate that the moderate to mild but prolonged reductions of CBF in kaolin-induced hydrocephalus may cause the delayed selective neuronal injury evidenced by the immunohistochemical changes that we saw in both the CA1 and CA3 subfields.…”

“…27 The authors found a disturbed long-term potentiation in CA1 neurons of the hippocampus and successfully demonstrated subtle morphological changes in the CA1 subfield using light microscopy and transmission electron microscopy. 28 Given that there are differences in the pathology of arteriovenous fistula-and kaolin-induced hydrocephalus, our observations on the neuronal response in the long-term stage of kaolin hydrocephalus strongly resembles the findings of arteriovenous fistula-induced ischemia.…”

Surgical Revascularization Reverses Cerebral Cortical Thinning in Patients With Severe Cerebrovascular Steno-Occlusive Disease

“…Experimental animal models simulating a state of nonischemic chronic hypoperfusion demonstrate a decline in neuronal structure and viability. 3,4 In humans, vascular cognitive impairment is associated with the loss of cortical gray matter, 5,6 whereas stenoocclusive disease without stroke has been associated with neurocognitive decline. 7,8 Looking at it from another perspective, neurodegenerative disorders such as Alzheimer disease 9,10 and Huntington disease 11 are associated with reduced vascular function.…”

Gene Transfer of Hepatocyte Growth Factor to Subarachnoid Space in Cerebral Hypoperfusion Model

“…Although such a condition leads to not only cerebral ischemic events, but also neuropathological changes including dementia, [1][2][3][4] an effective treatment for hypoperfusion has not yet been established. Ischemic stroke induces active angiogenesis, particularly in the ischemic penumbra, which correlates with longer survival in humans.…”