Hyperbaric oxygen therapy in experimental and clinical stroke - PubMed (original) (raw)
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Hyperbaric oxygen therapy in experimental and clinical stroke
Wei-Wei Zhai et al. Med Gas Res. 2016.
Abstract
Stroke, which is defined as a neurologic deficit caused by sudden impaired blood supply, has been considered as a common cause of death and disability for decades. The World Health Organization has declared that almost every 5 seconds a new stroke occurs, placing immense socioeconomic burdens. However, the effective and available treatment strategies are still limited. Additionally, the most effective therapy, such as thrombolysis and stenting for ischemic stroke, generally requires a narrow therapeutic time window after the event. A large majority of patients cannot be admitted to hospital and receive these effective treatments for reperfusion timely. Hyperbaric oxygen therapy (HBOT) has been frequently applied and investigated in stroke since 1960s. Numerous basic and clinical studies have shown the beneficial efficacy for neurological outcome after stroke, and meanwhile many underlying mechanisms associated with neuroprotection have been illustrated, such as cerebral oxygenation promotion and metabolic improvement, blood-brain barrier protection, anti-inflammation and cerebral edema, intracranial pressure modulation, decreased oxidative-stress and apoptosis, increased vascular and neural regeneration. However, HBOT in human stroke is still not sufficiently evidence-based, due to the insufficient randomized double-blind controlled clinical studies. To date, there are no uniform criteria for the dose and session duration of HBOT in different strokes. Furthermore, the additional effect of HBOT combined with drugs and other treatment strategies are being investigated recently. Therefore, more experimental and clinical research is imperative to identify the mechanisms more clearly and to explore the best protocol of HBOT in stroke treatment.
Keywords: cerebrovascular disease; clinical studies; experimental studies; hyperbaric oxygen preconditioning; hyperbaric oxygen therapy; ischemia; stroke.
Conflict of interest statement
The authors declare that they have no competing interests.
Figures
Figure 1
Possible mechanisms of hyperbaric oxygen therapy (HBOT) in stroke treatment. Note: BMSC: Bone marrow stem cell; PPARγ: peroxisome proliferator activated receptor-γ; VEGF: vascular endothelial growth factor; PKC-α: phospho-protein kinase C-alpha; TNF-α: tumor necrosis factor-alpha; MMP: matrix metalloproteinases; HIF-1α: hypoxia-inducible factor-1α; COX-2: cyclooxygenase-2; BBB: blood-brain barrier; SAH: subarachnoid hemorrhage.
Figure 2
The common clinical application of hyperbaric oxygen therapy (HBOT) in stroke. Note: SAH: Subarachnoid hemorrhage; ICH: intracerebral hemorrhage.
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