The effect of hyperbaric oxygen on nitric oxide synthase activity and expression in ischemia-reperfusion injury

Baynosa, Richard C.; Naig, Anna L.; Murphy, Patrick S.; Fang, Xin; Stephenson, Linda L.; Khiabani, Kayvan T.; Wang, Wei Z.; Zamboni, William A.

doi:10.1016/j.jss.2013.01.004

Cited by 25 publications

(22 citation statements)

References 38 publications

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“…12,13 Using rat pedicle skeletal muscle flaps, it was shown that neutrophil adhesion to endothelial cells through neutrophil beta-2-integrin CD18 surface molecule was also inhibited by HBO in a NO-dependent manner. 14,15 Microvascular vasoconstriction was also reversed following HBO. Conversely, it is well known that HBO induces vasoconstriction.…”

Section: Mechanisms Of Actionmentioning

confidence: 95%

Hyperbaric Oxygen Therapy for the Compromised Graft or Flap

Francis

Baynosa

2017

Advances in Wound Care

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Tissue grafts and flaps are used to reconstruct wounds from trauma, chronic disease, tumor extirpation, burns, and infection. Despite careful surgical planning and execution, reconstructive failure can occur due to poor wound beds, radiation, random flap necrosis, vascular insufficiency, or ischemia-reperfusion (IR). Traumatic avulsions and amputated composite tissues-compromised tissue-may fail from crush injury and excessively large sizes. While never intended, these complications result in tissue loss, additional surgery, accrued costs, and negative psychosocial patient effects. Hyperbaric oxygen (HBO) has demonstrated utility in the salvage of compromised grafts/flaps. It can increase the likelihood and effective size of composite graft survival, improve skin graft outcomes, and enhance flap survival. Mechanisms underlying these beneficial effects include increased oxygenation, improved fibroblast function, neovascularization, and amelioration of IR injury. Common strategies for the compromised graft or flap include local wound care, surgical debridement, and repeated reconstruction. These modalities are associated with added costs, time, need for reoperation, morbidity, and psychosocial effects. Preservation of the amputated/avulsed tissues minimizes morbidity and maximizes the reconstructive outcome by salvaging the compromised tissue and obviating additional surgery. HBO is often overlooked as a potential tool that can limit these issues. Animal studies demonstrate a benefit of HBO in the treatment of compromised tissues. Clinical studies support these findings, but are limited to case reports and series. Further research is needed to provide multicenter prospective clinical studies and cost analyses comparing HBO to other adjunctive therapies in the treatment of compromised grafts/flaps.

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Section: Mechanisms Of Actionmentioning

confidence: 95%

Hyperbaric Oxygen Therapy for the Compromised Graft or Flap

Francis

Baynosa

2017

Advances in Wound Care

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“…In the past 2 decades, Thom, 34 Piantadosi and colleagues, 36–38 Zamboni and colleagues, 39,40 and others have elucidated the biochemical basis for HBOT, the principal mechanism of which is the controlled generation of reactive oxygen and nitrogen species. 1,34 These increases result in higher levels of various growth factors and the activation of growth factor receptors, the mobilization of bone-marrow-derived stem/progenitor cells, an alteration in the function of integrin (resulting in reduced neutrophil adhesion), and changes in monocyte chemokine synthesis, as well as hemoxygenase-1, heat shock proteins, and hypoxia-inducible factor-1 that reduce inflammation.…”

Section: Indications and Mechanism Of Actionmentioning

confidence: 99%

An Update on the Appropriate Role for Hyperbaric Oxygen: Indications and Evidence

Fife

Eckert

Carter

2016

Plastic &Amp; Reconstructive Surgery

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Background:Among advanced therapeutic interventions for wounds, hyperbaric oxygen therapy (HBOT) has the unique ability to ameliorate tissue hypoxia, reduce pathologic inflammation, and mitigate ischemia reperfusion injury. Most of the conditions for which it is utilized have few successful alternative treatments, and the morbidity and mortality associated with treatment failure are significant. Data on the efficacy and effectiveness of HBOT were reviewed, comparative effectiveness research of HBOT was explained, and a new paradigm for the appropriate use of HBOT was described.Methods:Systematic reviews and randomized controlled trials that have evaluated HBOT were reviewed.Results:Although numerous small randomized controlled trials provide compelling support for HBOT, the physics of the hyperbaric environment create significant barriers to trial design. The electronic health record infrastructure created to satisfy mandatory quality and registry reporting requirements as part of healthcare reform can be harnessed to facilitate the acquisition of real world data for HBOT comparative effectiveness studies and clinical decision support.Conclusions:Predictive models can identify patients unlikely to heal spontaneously and most likely to benefit from HBOT. Although electronic health records can automate the calculation of predictive models making them available at the point of care, using them in clinical decision making is complicated. It is not clear whether stakeholders will support the allocation of healthcare resources using mathematical models, but the current patient selection process mandates a 30-day delay for all patients who might benefit and allows treatment for at least some patients who cannot benefit.

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“…Nonetheless, recent studies have reported that hyperoxygenation with 100% O 2 at 2–3 atmospheres absolute (ATA) is beneficial for treating various brain disorders (Yan, Liang, & Cheng, ). Hyperoxygenation treatment improved cognitive sequelae in patients with carbon monoxide poisoning (Weaver et al, ) and ameliorated traumatic brain injury (Huang & Obenaus, ) and ischemic brain injury (Baynosa et al, ). Furthermore, hyperoxygenation treatment (100% O 2 , 2.5 ATA), with 30 intermittent exposures, improved cognitive function in elderly individuals with cognitive deficits (Jacobs, Winter, Alvis, & Small, ).…”

Section: Introductionmentioning

confidence: 99%

Hyperoxygenation revitalizes Alzheimer’s disease pathology through the upregulation of neurotrophic factors

et al. 2019

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Alzheimer’s disease (AD) is a neurodegenerative disease characterized by Aβ‐induced pathology and progressive cognitive decline. The incidence of AD is growing globally, yet a prompt and effective remedy is not available. Aging is the greatest risk factor for AD. Brain aging proceeds with reduced vascularization, which can cause low oxygen (O2) availability. Accordingly, the question may be raised whether O2 availability in the brain affects AD pathology. We found that Tg‐APP/PS1 mice treated with 100% O2 at increased atmospheric pressure in a chamber exhibited markedly reduced Aβ accumulation and hippocampal neuritic atrophy, increased hippocampal neurogenesis, and profoundly improved the cognitive deficits on the multiple behavioral test paradigms. Hyperoxygenation treatment increased the expression of BDNF, NT3, and NT4/5 through the upregulation of MeCP2/p‐CREB activity in HT22 cells in vitro and in the hippocampus of mice. In contrast, siRNA‐mediated inhibition of MeCP2 or TrkB neurotrophin receptors in the hippocampal subregion, which suppresses neurotrophin expression and neurotrophin action, respectively, blocked the therapeutic effects of hyperoxygenation on the cognitive impairments of Tg‐APP/PS1 mice. Our results highlight the importance of the O2‐related mechanisms in AD pathology, which can be revitalized by hyperoxygenation treatment, and the therapeutic potential of hyperoxygenation for AD.

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The effect of hyperbaric oxygen on nitric oxide synthase activity and expression in ischemia-reperfusion injury

Cited by 25 publications

References 38 publications

Hyperbaric Oxygen Therapy for the Compromised Graft or Flap

Hyperbaric Oxygen Therapy for the Compromised Graft or Flap

An Update on the Appropriate Role for Hyperbaric Oxygen: Indications and Evidence

Hyperoxygenation revitalizes Alzheimer’s disease pathology through the upregulation of neurotrophic factors

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