ArticleNeurochemical research2002
Chronic cerebral hypoperfusion induces striatal alterations due to the transient increase of NO production and the depression of glutathione content.
Article in Neurochemical research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 16 citations in OpenAlex.
- Detecting Key Functional Components Group and Speculating the Potential Mechanism of Xiao-Xu-Ming Decoction in Treating Stroke.Frontiers in cell and developmental biology · 2022Article
- Article
- Bilateral common carotid artery ligation transiently changes brain lipid metabolism in rats.Neurochemical research · 2012Article
- AT1 receptor blocker candesartan-induced attenuation of brain injury of rats subjected to chronic cerebral hypoperfusion.Neurochemical research · 2007Article
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Authors and funding
5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We examined the effects of chronic cerebral hypoperfusion on the endogenous oxidative stress-related indices, nitrite and nitrate (NOx) concentration, glutathione (GSH) content, superoxide dismutase and catalase activities, and thiobarbituric acid-reactive substances level in the rat striatum, to clarify the participation of oxidative stress in the chronic cerebral hypoperfusion-induced alterations. Our present results indicate that chronic cerebral hypoperfusion produces oxidative stress and disturbs intracellular redox regulation in two distinct phases: at 1 day, "acute" and at 6 weeks, "chronic" alterations after the operation. Therefore, striatal neural cell damage may be mainly attributed to the transient increase of NOx production at 1 day after, and the delayed reduction of muscarinic acetylcholine receptor binding in the striatum may be mostly attributed to the continuous depression of GSH content from the 1st to the 6th postoperative week. In particular, the continuous GSH depression may be considered to accompany the pathophysiology of chronic cerebral hypoperfusion.
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