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REVIEW ARTICLE
Year : 2015  |  Volume : 1  |  Issue : 1  |  Page : 97-103

Cerebrovascular ischemic protection by pre- and post-conditioning


Department of Neurosurgery; Department of Cell Biology and Physiology; Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri, USA

Correspondence Address:
Jeffrey M Gidday
Department of Neurosurgery, Washington University School of Medicine, Box 8057, St. Louis, Missouri - 63110
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2394-8108.166379

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Stroke and cardiac arrest involve injury to all the brain's resident cells and their respective progenitors, including neurons, all glial subtypes, vascular smooth muscle, vascular endothelium, and pericytes, resulting either in the death of the individual or in a lesion that likely manifests as long-term impairments across a number of cognitive and functional domains. Thousands of studies in experimental animals and results from a few clinical trials in humans have demonstrated that the mechanisms responsible for ischemic brain injury can be blocked or slowed by survival-enhancing epigenetic responses induced by "conditioning" the brain with a stress stimulus paradigm before or even after ictus. The resultant reduction in lesion size and functional deficits are often termed endogenous "neuroprotection," but this in fact involves cytoprotective responses on the part of all the aforementioned resident brain cells and the circulating immune cells as well. The present review will summarize findings demonstrating conditioning-induced protection of the cerebral vasculature, that in turn manifests as reductions in vascularly targeted inflammatory responses; less endothelial injury and improvements in structural integrity of the circulation across all levels of organization; enhanced perfusion with less thrombosis; reductions in vascular dysregulation and reactivity impairments; and, over the longer term, more robust angiogenesis and vascular remodeling. Advancing the mechanistic basis for these innately vasculoprotective phenotypes may provide therapeutic targets for limiting cerebral circulatory injury and dysfunction following stroke and cardiac arrest.


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