Abstract
Hyperbaric oxygen therapy (HBOT) is a clinical treatment in which a patient breathes pure oxygen for a limited period of time at an increased pressure. Although this therapy has been used for decades to assist wound healing, its efficacy for many conditions is unproven and its mechanism of action is not yet fully clarified. This study investigated the effects of HBOT on wound healing using a diabetes-impaired pressure ulcer rat model. Seven weeks after streptozotocin-induced diabetes in rats (n = 55), a pressure ulcer was created on dorsal skin. Subsequently, animals received HBOT during 6 weeks following a standard clinical protocol (HBOT group with varying endpoints up to 42 days post-wounding) versus controls without HBOT. Capillary venous oxygen saturation (SO2) showed a significant increase in the HBOT group on day 24; however, this increase was significant at this time point only. The quantity of hemoglobin in the micro-blood vessels (rHB) showed a significant decrease in the HBOT group on days 21 and 42, and showed a trend to decrease on day 31. Blood flow in the microcirculation showed a significant increase on days 17, 21 and 31 but a significant decrease on days 24 and 28. Inflammation scoring showed significantly decreased CD68 counts in the HBOT group on day 42, but not in the early stages of wound healing. Animals in the HBOT group showed a trend for an increase in mean wound breaking strength on day 42.
Highlights
The treatment of impaired wound healing remains a challenge
A separate, free radical-based mechanism for the augmentation of neovascularization by Hyperbaric oxygen therapy (HBOT) is through circulating stem/progenitor cells (SPCs)
The experimental protocol was approved by an Animal Experiments Committee (Stichting Dec-Consult, the Netherlands), under the National Experiments on Animals Act and adhered to the rules laid down in this national law that serves the implementation of Guidelines on the Protection of Experimental Animals by the Council of Europe (1986), Directive 86/609/EC
Summary
The treatment of impaired wound healing remains a challenge. Various biological processes, such as chronic inflammation, hampered keratinocyte functioning, and abnormalities in growth factor production, extracellular matrix deposition and in the tissue remodeling process, are proposed to contribute to compromised diabetes-impaired wound healing [1,2,3,4].Hyperbaric oxygen therapy (HBOT) is a clinical treatment modality in which a patient breathes pure oxygen while exposed to an increased atmospheric pressure of (generally) 2.4 atmospheres absolute (ATA) [5, 6]. The treatment of impaired wound healing remains a challenge. Various biological processes, such as chronic inflammation, hampered keratinocyte functioning, and abnormalities in growth factor production, extracellular matrix deposition and in the tissue remodeling process, are proposed to contribute to compromised diabetes-impaired wound healing [1,2,3,4]. HBOT and diabetes impaired wounds reduce the risk of lower extremity amputation, with the aim to improve quality of life and reduce the overall costs of care [7, 8]. After HBOT, cells in the wound area exhibit increased growth factor production and neovascularization, as well as improved cell migration and collagen synthesis. A separate, free radical-based mechanism for the augmentation of neovascularization by HBOT is through circulating stem/progenitor cells (SPCs). Hyperoxia stimulates mobilization of bone marrow SPCs and improves their function once they home to peripheral sites [9]
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