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Normobaric Hyperoxia Slows Blood–Brain Barrier Damage and Expands the Therapeutic Time Window for Tissue-Type Plasminogen Activator Treatment in Cerebral Ischemia
Author(s) -
Jia Liang,
Zhifeng Qi,
Wenlan Liu,
Peng Wang,
Wenjuan Shi,
Wen Dong,
Xunming Ji,
Yumin Luo,
Ke Jian Liu
Publication year - 2015
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.114.008599
Subject(s) - medicine , ischemia , blood–brain barrier , tissue plasminogen activator , pathogenesis , occludin , anesthesia , plasminogen activator , pharmacology , tight junction , central nervous system , biology , microbiology and biotechnology
Prolonged ischemia causes blood-brain barrier (BBB) damage and increases the incidence of neurovasculature complications secondary to reperfusion. Therefore, targeting ischemic BBB damage pathogenesis is critical to reducing neurovasculature complications and expanding the therapeutic time window of tissue-type plasminogen activator (tPA) thrombolysis. This study investigates whether increasing cerebral tissue PO2 through normobaric hyperoxia (NBO) treatment will slow the progression of BBB damage and, thus, improve the outcome of delayed tPA treatment after cerebral ischemia.

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