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• W69798544 abstract "Secondary brain damage is tissue injury that is not apparent immediately after an insult, but develops after a delay of hours or days and has typically been observed after ischemia, trauma or subarachnoidal haemorrhage [1]. Secondary ischemic brain damage develops as a consequence of: (a) brain edema, (b) post-ischemic microvascular stasis and vasomotor/hemodynamic deficits leading to hypoperfusion, and (c) post-ischemic inflammation involving activation of microglia and brain infiltration of peripheral inflammatory cells [1–3]. It is believed that damage to the tissues surrounding the ischemic core, known as the penumbra, can be reduced by therapeutic measures designed to prevent or minimize molecular events contributing to the development of secondary brain damage [3]." @default.
• W69798544 created "2016-06-24" @default.
• W69798544 creator A5043006925 @default.
• W69798544 date "2001-01-01" @default.
• W69798544 modified "2023-09-28" @default.
• W69798544 title "Mediators of inflammation and blood-brain barrier permeability in cerebral ischemia" @default.
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• W69798544 doi "https://doi.org/10.1007/978-3-0348-8297-2_19" @default.
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