Ischemic Tissue Oxygen Capacitance after Hyperbaric Oxygen Therapy: A New Physiologic Concept

Abstract

In an effort to better understand the effects of hyperbaric oxygen therapy on ischemic tissue, we monitored the real-time changes in subcutaneous tissue oxygen tension before, during, and after exposure to hyperbaric oxygen treatments. We identified an elevation of the tissue oxygen partial pressure to over 300 mmHg during the treatment period (up from a baseline mean of 24 mmHg) in a sustained ischemia rabbit ear model (n = 22 rabbits). There was no sustained change in tissue oxygen tension beyond the period of treatment. This manner of response is consistent with several current theories used to explain the mechanism of action of hyperbaric oxygen therapy. It is also consonant with our opinion that molecular oxygen, when delivered at high pressure, can function both as a respiratory metabolite and as a signal transducer. We also studied the impact of nontherapeutic 100% oxygen at 1 atm on tissue. The sustained peak tissue oxygen tension during such challenges increased in direct proportion to the number of hyperbaric oxygen treatments given. The clinical relevance and extension of these findings are discussed.

Hyperbaric oxygen protects from sepsis mortality via an interleukin-10–dependent mechanism*

“…However, increases in tissue PO 2 are transient and decline rapidly after HBO 2 exposure (26,27). Furthermore, we did not observe an improvement in IL10 -/-vs. IL-10 ϩ/ϩ mice during our study.…”

Hyperbaric Oxygen Therapy Mediates Increased Nitric Oxide Production Associated With Wound Healing

“…[1][2][3][4] Hyperoxia during HBOT is an important mediating factor for wound collagen deposition and cross-linking, 5 neutrophil-dependent microbial killing, 6 and neovascularization. 7 Other HBOT-mediated processes in wound healing include the inhibition of integrin-mediated intravascular leukocyte adhesions and platelet aggregation, 8 enhancement of cutaneous microvascular homeostasis after ischemia-reperfusion syndrome, 9 increased oxygen capacitance and survival of ischemic flaps, 10 and upregulation of platelet-derived growth factor (PDGF) receptor mRNA. 11 Experimental normobaric oxygen activates gene expression in human dermal fibroblasts, supporting the concept of oxygen as a possible signal transducer.…”

Oxygen in wound healing: More than a nutrient

“…Under controlled experimental conditions in vivo, we were able to show in young and aged ischemic rabbit ear ulcers that wound healing is delayed under hypoxia as a result of reduced granulation tissue production and delayed epithelialization [3,4]. Ischemic ears in this rabbit ear model have tissue oxygen tensions of approximately 24 mmHg versus the level of 53 mmHg measured in non-ischemic ears [5].…”

“…Also, the baseline levels of tissue oxygen tensions increased from 24 mmHg to 32 mmHg after 14 days of HBO treatment versus an unchanged 53 mmHg in the nonischemic ear. These changes are most likely a result of enhanced neovascularization under HBO treatment [5]. In the same model, oxygen delivery at 1 atm pressure (100% O 2 or NBO) had no therapeutic effect.…”