Mechanisms of hyperbaric oxygen and neuroprotection in stroke

Zhang, Junyi; Lo, Takkin; Mychaskiw, George; Colohan, Austin R. T.

doi:10.1016/j.pathophys.2005.01.003

Cited by 92 publications

(93 citation statements)

References 126 publications

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“…Ischemic strokes include focal and global cerebral ischemia, which reduce regional blood flow to affected regions and cause hypoxia-ischemia, with consequent activation of pathogenic cascades, with eventual neuronal deficit and cell damage (33). Many drugs have been evaluated for ameliorating neurological outcomes associated with cerebral ischemic strokes.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Potentials of an Artificial Oxygen-Carrier, Liposome-Encapsulated Hemoglobin, for Ischemia/Reperfusion-Induced Cerebral Dysfunction in Rats

et al. 2010

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Abstract. We performed this study to elucidate whether a newly developed liposome-encapsulated hemoglobin, TRM-645 (TRM), can prevent cerebral dysfunction resulting from acute ischemic stroke when used as an oxygen carrier. Hippocampal long-term potentiation (LTP) in the perforant path-dentate gyrus synapses and anxiety-related behaviors in the elevated plus-maze test were evaluated as indices of cerebral functional outcomes in the rat with two-vessel occlusion (2VO), which was induced by 10-min clamping of bilateral common carotid arteries. Saline or TRM (hemoglobin concentration of 6 g/dl: 2.5 or 5 ml/kg) was administered via the tail vein immediately after ischemic insult. Hippocampal LTP formation was markedly impaired and the open arm durations in the elevated plus-maze decreased significantly 4 days after 2VO, compared to those of sham-operated (control) rats, suggesting the hippocampal synaptic dysfunction and anxiogenic properties in 2VO rats. TRM (5 ml/kg) restored the hippocampal LTP formation and normalized the anxiety-related behavior. TRM also improved the decreased tissue oxygen partial pressure in the 2VO rat hippocampus, possibly due to oxygen delivery to ischemic regions. Liposomeencapsulated hemoglobin TRM might have therapeutic potentials for protecting the brain from neurological complications associated with acute ischemic stroke, as a promising blood substitute for oxygen therapy.

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Section: Discussionmentioning

confidence: 99%

Therapeutic Potentials of an Artificial Oxygen-Carrier, Liposome-Encapsulated Hemoglobin, for Ischemia/Reperfusion-Induced Cerebral Dysfunction in Rats

et al. 2010

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“…HBOT is a treatment in which oxygen-enriched air (up to 100%) is administrated to patients in a chamber where the pressure is elevated above one atmosphere absolute (1ATA), which is the ambient atmospheric pressure). It is becoming widely acknowledged that the combined action of hyperoxia and hyperbaric pressure leads to significant improvement in tissue oxygenation while targeting both oxygenand pressure-sensitive genes [3][4][5][6], resulting in improved mitochondrial metabolism with anti-apoptotic and anti-inflammatory effects [7][8][9][10][11][12].…”

Section: New Hopementioning

confidence: 99%

“…The decreased oxygen level not only causes reduction in neuronal activity but also prevents the generation of new synaptic connections and angiogenesis. HBOT can initiate vascular repair and improve cerebral vascular flow, induce regeneration of axonal white matter, stimulate axonal growth, promote blood-brain barrier integrity and reduce inflammatory reactions as well as brain edema [7][8][9][10][11][12].…”

Section: Underlying Repair Mechanismsmentioning

confidence: 99%

“…At the cellular level, HBOT can improve cellular metabolism, reduce apoptosis, alleviate oxidative stress and increase levels of neurotrophins and nitric oxide through enhancement of mitochondrial function in both neurons and glial cells, and may even promote neurogenesis of endogenous neural stem cells [7][8][9][10][11][12]14]. Regarding mitochondria, it is important to note that stroke and TBI engender depolarization of the mitochondria membrane and induction of mitochondrial permeability transition pore, which reduces the efficiency of energy production and elevate the level of reactive oxygen species [15].…”

Section: Underlying Repair Mechanismsmentioning

confidence: 99%

“…However, this will require novel basic biomedical research to understand the HBOT effect on the recently discovered mitochondria-associated cellular response to hypoxia [7][8][9][10][11][12], which is a common denominator of stroke, TBI, dementia and aging [25,26].…”

Section: Looking Aheadmentioning

confidence: 99%

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