Research reportDisruption of the blood-cerebrospinal fluid barrier by transient cerebral ischemia
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Toward changing of the pathophysiologic basis of acute hydrocephalus after subarachnoid hemorrhage: A preliminary experimental study
2013, World NeurosurgeryCitation Excerpt :CP are located in the ventricles and composed of highly vascularized villi covered by a ciliated modified ependymal epithelium (2, 8). They are highly vulnerable to damage in head injuries (27), infections (36), and ischemic conditions (30). In our study, we observed the fluid-filled vesicles in CP in the acute period after SAH, so it was shown that SAH has a fluid-producing effect on the epithelial cells of the CP.
Quantitative evaluation of blood-cerebrospinal fluid barrier permeability in the rat with experimental meningitis using magnetic resonance imaging
2010, Brain ResearchCitation Excerpt :Moreover, GER showed the protective effect of prednisolone on the BCSFB disruption induced by IL-1β. The permeability of the BCSFB in previous studies has been evaluated by the signal intensity of Gd–DTPA enhanced T1W images or by the T1 value of CSF after administration of Gd–DTPA (Nagahiro et al., 1994; Meltzer et al., 1996; Thwaites et al., 2007). In addition, Gd–DTPA has been reported to be useful to visualize the changes in the BBB permeability in meningitis and the lung permeability in pneumonia (Spellerberg et al., 1995; Idänpään-Heikkilä et al., 1997).
Volume Transmission-Mediated Protective Impact of Choroid Plexus-Cerebrospinal Fluid Growth Factors on Forebrain Ischemic Injury
2004, Blood-Spinal Cord and Brain Barriers in Health and DiseaseTemporal effects of left versus right middle cerebral artery occlusion on spleen lymphocyte subsets and mitogenic response in Wistar rats
2002, Brain ResearchCitation Excerpt :The local cerebral immune and inflammatory responses to stroke involve upregulation of several inflammatory mediators, including cytokines, chemokines, cell adhesion molecules, and reactive oxygen and nitrogen species that contribute to neuronal damage [1,23]. Such mediators are released by resident cells (e.g. microglia, astrocytes), and by peripherally-derived leukocytes infiltrating the CNS following disruption of the blood–brain barrier, and exposure of relatively sequestered CNS antigens to the peripheral circulation [24,26,28,31,40,56–58]. Impairment and lateralization of immune function in the periphery are likely to occur after ischemic stroke, given the reported asymmetries of stroke-induced sympathetic consequences and the important role of the sympathetic nervous system in immune regulation.
Cell proliferation and differentiation from ependymal, subependymal and choroid plexus cells in response to stroke in rats
2002, Journal of the Neurological Sciences