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Normobaric hyperoxia-based neuroprotective therapies in ischemic stroke

Zhifeng Qi1, Wenlan Liu23, Yumin Luo1, Xunming Ji1 and Ke Jian Liu13*

Author Affiliations

1 Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China

2 Central Laboratory of Shenzhen 2nd People’s Hospital, the 1st Affiliated Hospital of Shenzhen University, 3002 Sungang West Rd, Shenzhen, Guangdong, 518035, China

3 Department of Pharmaceutical Sciences, University of New Mexico Health Sciences Center, Albuquerque, NM, 87131, USA

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Medical Gas Research 2013, 3:2  doi:10.1186/2045-9912-3-2

Published: 9 January 2013


Stroke is a leading cause of death and disability due to disturbance of blood supply to the brain. As brain is highly sensitive to hypoxia, insufficient oxygen supply is a critical event contributing to ischemic brain injury. Normobaric hyperoxia (NBO) that aims to enhance oxygen delivery to hypoxic tissues has long been considered as a logical neuroprotective therapy for ischemic stroke. To date, many possible mechanisms have been reported to elucidate NBO’s neuroprotection, such as improving tissue oxygenation, increasing cerebral blood flow, reducing oxidative stress and protecting the blood brain barrier. As ischemic stroke triggers a battery of damaging events, combining NBO with other agents or treatments that target multiple mechanisms of injury may achieve better outcome than individual treatment alone. More importantly, time loss is brain loss in acute cerebral ischemia. NBO can be a rapid therapy to attenuate or slow down the evolution of ischemic tissues towards necrosis and therefore “buy time” for reperfusion therapies. This article summarizes the current literatures on NBO as a simple, widely accessible, and potentially cost-effective therapeutic strategy for treatment of acute ischemic stroke.

Oxygen; Ischemia; Oxidative stress; Blood brain barrier; Reperfusion; Blood flow; Neuroprotection