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Proposed mechanisms for (A) microparticle-induced dysfunction of autoregulatory hypotensive cerebrovasodilation after traumatic brain injury and (B) protection of autoregulatory hypotensive cerebrovasodilation via polyethylene glycol telomere B (PEG-TB). TBI, traumatic brain injury; tPA, tissue plasminogen activator; ET-1, endothelin-1; pERK MAPK, phospho extracellular signal-regulated kinases-mitogen activated protein kinase.
