Abstract

Molecular oxygen (O2) is a vital element in human survival and plays a major role in a diverse range of biological and physiological processes. Although normobaric hyperoxia can increase arterial oxygen content ([Formula: see text]), it also causes vasoconstriction and hence reduces O2 delivery in various vascular beds, including the heart, skeletal muscle, and brain. Thus, a seemingly paradoxical situation exists in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Nevertheless, with various degrees of effectiveness, and not without consequences, supplemental oxygen is used clinically in an attempt to correct tissue hypoxia (e.g., brain ischemia, traumatic brain injury, carbon monoxide poisoning, etc.) and chronic hypoxemia (e.g., severe COPD, etc.) and to help with wound healing, necrosis, or reperfusion injuries (e.g., compromised grafts). Hyperoxia has also been used liberally by athletes in a belief that it offers performance-enhancing benefits; such benefits also extend to hypoxemic patients both at rest and during rehabilitation. This review aims to provide a comprehensive overview of the effects of hyperoxia in humans from the "bench to bedside." The first section will focus on the basic physiological principles of partial pressure of arterial O2, [Formula: see text], and barometric pressure and how these changes lead to variation in regional O2 delivery. This review provides an overview of the evidence for and against the use of hyperoxia as an aid to enhance physical performance. The final section addresses pathophysiological concepts, clinical studies, and implications for therapy. The potential of O2 toxicity and future research directions are also considered.

Highlights

  • Molecular oxygen (O2) is one of the most important elements on Earth, for aerobic organisms that depend on it to release energy from carbon-based molecules

  • Ary injury is due to a variety of factors, including a compromise in cerebral autoregulation, microcirculatory dysfunction, reperfusion injury, hypoxemia, hyperthermia, unstable PaCO2, concomitant anemia, and hyperoxia. These factors have been covered in greater detail elsewhere [243], we briefly summarize the utility of hyperoxia in the treatment of hypoxic ischemic brain injury (HIBI)

  • The following question arises: is there a clear role for O2 therapy to improve exercise performance and capacity in patients with chronic obstructive pulmonary disease (COPD) and other hypoxemic pathologies? other therapeutic approaches such as noninvasive ventilatory support and low-density gases have been successfully employed as nonpharmacological adjuncts to exercise training to enhance the ability of patients with COPD to exercise, we focus on the putative benefits of supplemental O2 [92, 257]

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Summary

INTRODUCTION

Molecular oxygen (O2) is one of the most important elements on Earth, for aerobic organisms that depend on it to release energy from carbon-based molecules. Hyperoxia induces a reduction in blood flow, thereby counteracting the benefits of increased CaO2 This hyperoxia-induced vasoconstriction has been observed in various vascular beds, including the heart [97, 158], skeletal muscle [64, 209], and brain [293], and can reach levels ϳ30% lower at a PaO2 of 420 mmHg [237]. The individuals participating in such studies often present with cardiac diseases, such as coronary artery disease (CAD) and congestive heart failure (CHF), to combine research data collection with routine clincical diagnostic tests The evidence from such tests overwhelmingly demonstrates that while breathing hyperoxic gas mixtures, coronary blood flow, measured via catheterization, is reduced compared with normal air [105, 171, 178, 179]. HBO seems to be the preferred choice to treat DCS, but NBO has the advantage of being more readily available and is sufficient to wash out inert gases from the body, at least initially

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