Antioxidant Response of Chronic Wounds to Hyperbaric Oxygen Therapy (original) (raw)
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Journal of Physics: Conference Series, 2017
Wound healing is a physiological process that occurs progressively through overlapping phases. Tissue oxygenation is an important part of the complex regulation for wound healing. Hyperbaric Oxygen (HBO) therapy is a method of increasing oxygen delivery to tissues. The therapy improves tissue oxygenation and stimulates the formation of H2O2 as a secondary messenger for Tumour Necrosis Factor alpha (TNF α), e-NOS, VEGF and Nuclear Factor Kappa Beta phosphorylation (NF-Kb) which play an important role in the rapid transcription of a wide variety of genes in response to extracellular stimuli. This study aims to determine the effects of Hyperbaric Oxygen therapy in enhancing the expressions of e-NOS, TNF-α, VEGF and wound healing. This study is an animal study with a 'randomized control group of pre-test and post test design' on 28 Wistar rats. Randomly, the rats were divided into 4 groups with 7 rats in each group. The HBO treatment group 1 received 5 sessions of HBO 2.4 ATA in 3x30 minutes; the HBO treatment group 2 received 10 sessions of HBO 2.4 ATA in 3x30 minutes; and each of the control groups were without HBO. Each of the 28 male rats were given a full thickness excisional wound of 1x1cm. Examinations of e-NOS, TNF-α, VEGF expressions and wound healing were performed on day-0 (pre-HBO) and day-5 HBO or on day-0 (pre-HBO) and day-10 HBO.The resultsshowthat the Hyperbaric Oxygen therapy can improve e-NOS (p=0.02), TNF-α (p= 0.02), VEGF expression (p=0.02) and wound healing (p=0.002) significantly in the provision of HBO 2.4 ATA for 3x30 minutes in 5 sessions over 5 consecutive days. While the 10 sessions of HBO 2.4 ATA for 3x30 minutes over 10 consecutive days only increase e-NOS (p=0.02), TNF-α (p=0.04), VEGF expression significantly (p=0.03) but do not improve wound healing significantly (p=0.3) compared with no HBO. The study concludes that HBO can improve the expressions of e-NOS, TNF-α, VEGF and wound healing in the provision of HBO 2.4 ATA for 3x30 minutes in 5 sessions, while the 10 sessions of HBO 2.4 ATA for 3x30 minutes only increase e-NOS, TNF-α, VEGF expression but do not improve wound healing.
In vivo effect of hyperbaric oxygen on wound angiogenesis and epithelialization
Wound Repair and Regeneration, 2009
Hyperbaric oxygen (HBO) therapy is increasingly being used in different areas of medical practice. While demonstrated to be effective in several settings, its mechanism of action is not well understood. In the present study, we determined the effects of HBO on wound epithelialization and neovascularization in an in vivo hairless mouse ear ''impaired'' wound model. To impair wound healing, macrophages were depleted by pretreatment with iota-carrageenan. Wound epithelialization and neovascularization were measured using intravital microscopy and computerized planimetry. Metalloproteinase-2 (MMP-2), MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and tumor necrosis factor-a (TNF-a) were measured on days 2 and 7 using immunohistochemistry. In nonimpaired healing wounds, the rate of epithelialization and neovascularization was significantly accelerated in the groups treated with HBO. Time to wound closure was significantly delayed in impaired compared with nonimpaired healing wounds and HBO treatment completely reversed this delay. Neither HBO treatment nor macrophage depletion caused significant alterations in MMP-2 expression in wounds. In contrast, TNF-a, MMP-9, and TIMP-1 were significantly up-regulated in the impaired healing group receiving HBO treatment. These results show that HBO therapy effectively reversed the negative effect exerted by macrophage reduction on wound epithelialization and neovascularization. This beneficial effect could be due to stimulation of TNF-a production and, to a lesser degree due to release of metalloproteinases.
Experimental Cell Research, 2012
Hyperbaric oxygen (HBO) therapy involves the inhalation of 100% oxygen, whilst inside a chamber at greater than atmospheric pressure. It is an effective treatment for chronic diabetic wounds, although the molecular mechanisms involved remain unclear. We hypothesised that HBO could alter inflammatory gene expression in human endothelial cells via a reactive oxygen/nitrogen speciesmediated pathway. Endothelial cells were exposed to a chronic wound model comprising hypoxia (2% O 2 at 1 atmosphere absolute (ATA); PO 2~2 kPa) in the presence of lipopolysaccharide and TNF-α for 24 h, then treated with HBO for 90 min (97.5% O 2 at 2.4 ATA; PO 2~2 37 kPa). 5 h post-HBO, 19
Safety and efficacy of hyperbaric oxygen therapy in chronic wound management: current evidence
Chronic Wound Care Management and Research, 2015
The breathing of pure oxygen under pressure to treat tissue damage has been employed for almost 45 years and has been investigated in prospective, retrospective, and randomized controlled trials. The physiological effects of oxygen treatment on wound tissue are profound, and include activation of immune cells, changes in cytokine production, and modulation of inflammatory and bactericidal mediators. Hyperbaric oxygen influences the biochemistry of whole cells, altering cell proliferation, angiogenesis, clotting, and tissue regeneration. The precise effects of hyperbaric oxygen on individual cell types and tissues are only beginning to be revealed in both animal and human studies. Many independent studies using hyperbaric oxygen adjunctively with standard wound care have observed improved healing, in particular for diabetic foot ulcers, and can result in a significant reduction in major amputations. Side effects occur infrequently, but myopia, ear barotrauma, and rarely oxygen toxicity have been reported. As antibiotics become less available, and clinician time and complex dressings become more expensive, use of hyperbaric oxygen as a means of treating a variety of wound types may become an increasingly appropriate option for treatment.
Oxygen in Wound Healing?More than a Nutrient
World Journal of Surgery, 2004
This article provides an overview of the role of oxygen in wound healing. The understanding of this role has undergone a major evolution from its long-recognized importance as an essential factor for oxidative metabolism, to its recognition as an important cell signal interacting with growth factors and other signals to regulate signal transduction pathways. Our laboratory has been engaged in thestudy of animal models of skin ischemia to explore in vivo the impact of hypoxia as well as the use of oxygen as a therapeutic agent either alone or in combination with other agents such as growth factors. We have demonstrated a synergistic effect of systemic hyperbaric oxygen and growth factors that has been substantiated by Hunt's group. Within the past 10 years research in the field of wound healing has given new insight into the mechanism of action of hypoxia and hyperoxia as modifiers of the normal time-course of wound healing. The article concludes with a discussion of why hypoxia and hyperoxia intercurrently play an important role in wound healing. Hypoxia-inducible factor 1 is crucial in that interplay.
Biochemical and Biophysical Research Communications, 2005
α-Lipoic acid (LA) has been found previously to accelerate wound repair in patients affected by chronic wounds who underwent hyperbaric oxygen (HBO) therapy. Because proteinases are important in wound repair, we hypothesized that LA may regulate matrix metalloproteinase (MMP) expression in cells that are involved in wound repair. Patients undergoing HBO therapy were double-blind randomized into two groups: the LA group and the placebo group. Gene expression profiles for MMPs and for angiogenesis mediators were evaluated in biopsies collected at the first HBO session, at the seventh HBO session, and after 14 days of HBO treatment. ELISA tests were used to validate microarray expression of selected genes. LA supplementation in combination with HBO therapy downregulated the inflammatory cytokines and the growth factors which, in turn, affect MMPs expression. The disruption of the positive autocrine feedback loops that maintain the chronic wound state promotes progression of the healing process.
Revisiting the essential role of oxygen in wound healing
The American Journal of Surgery, 2003
Hypoxemia, caused by disrupted vasculature, is a key factor that limits wound healing. Correcting hypoxemia through the administration of supplemental oxygen (O(2)) can have significant beneficial impact on wound healing in the perioperative and outpatient settings. Beyond its role as a nutrient and antibiotic, O(2) may support vital processes such as angiogenesis, cell motility, and extracellular matrix formation. Recent discoveries highlight a novel aspect, addressing the role of O(2) in wound healing via the production of reactive oxygen species (ROS). Almost all wound-related cells possess specialized enzymes that generate ROS (including free radicals and H(2)O(2)) from O(2). Defect in these enzymes is associated with impaired healing. Low wound pO(2) is expected to compromise the function of these enzymes. At low concentrations, ROS serve as cellular messengers to support wound healing. The use of systemic hyperbaric O(2) therapy presents potential advantages, as well as risks. There is evidence to suspect that the use of pressure and systemic pure O(2) may not be essential in wound care. Elimination of these factors by using sub-pure systemic O(2) under normobaric conditions may significantly minimize the risk of O(2) toxicity. Furthermore, opportunities to treat dermal wounds using topical O(2) therapy warrant further investigation. Given that many growth factors require ROS for their function, it is reasonable to assume that approaches to correct wound pO(2) will serve as an effective adjunct in treating chronic wounds.
Oxygen: Implications for Wound Healing
Advances in Wound Care, 2012
Background: Oxygen is vital for healing wounds. It is intricately involved in numerous biological processes including cell proliferation, angiogenesis, and protein synthesis, which are required for restoration of tissue function and integrity. Adequate wound tissue oxygenation can trigger healing responses and favorably influence the outcomes of other treatment modalities. The Problem: Chronic ischemic wounds fail to heal appropriately secondary to extreme hypoxia that leads to cellular demise. Wound tissue hypoxia is typically greater at the center of the wound. Accordingly, oxygen requirements of the regenerating tissue will vary. Basic/Clinical Science Advances: As oxygen levels decrease within the wound, cell response mechanisms (hypoxia inducible factor [HIF]) trigger the transcription of genes that promote cell survival and angiogenesis. HIF stabilizers are currently being tested to determine wound healing potential. Clinically, topical oxygen therapy (TOT) has been proved as an effective therapeutic modality for chronic wounds. TOT is reputed to have several advantages over hyperbaric oxygen therapy. Namely, TOT has a lower risk of oxygen toxicity, it is less expensive and is relatively easy to apply to target areas. Clinical Care Relevance: Wound tissue oxygen is necessary for appropriate wound healing; however, the relative complexity of the healing process requires a multifaceted approach for successful healing outcomes. A key component of this multifaceted approach should be specific oxygen dosing as a function of tissue hypoxia. Conclusion: New treatment approaches that exploit cell hypoxia sensing and response mechanisms and that enable the precise application of oxygen therapy to hypoxic areas of regenerating tissue are very promising. j 225