Background: Given the low physical solubility of oxygen (O2) in plasma, little value is attached to hyperoxic ventilation (FiO2 1.0) as a modality for improving O2 transport and tissue oxygen supply when hypoxemia (i.e., O2 partial pressure (paO2) <60 mmHg) is absent. Because recent experimental and clinical data conflict with this notion, we used mathematical modeling to reevaluate efficacy of hyperoxic ventilation in improving tissue oxygenation in the absence of hypoxemia by specifying its theoretical efficacy in terms of hemoglobin (Hb) equivalents.
Methods: A mathematical approach was used based on the assumption that efficacy of hyperoxic ventilation depends on the additional amount of O2 dissolved in plasma and is influenced by the high biological availability of the additional O2 provided at high paO2. This approach was used to calculate the amount of additional Hb necessary to increase the amount of utilizable O2 to the same extent as hyperoxic ventilation (the so-called "Hb equivalent").
Results: Although former estimations strongly underestimated efficacy of hyperoxic ventilation (Hb equivalent, 1-2 g/dL), our more exact mathematical approach revealed a theoretical Hb equivalent of hyperoxic ventilation in the range of 3-7 g/dL, which depended on basic physiological conditions like pulmonary function, Hb concentration, and peripheral shunt perfusion.
Conclusion: Hyperoxic ventilation establishes a highly available source of O2 that can be utilized effectively for tissue oxygenation. Although further experimental studies are required to quantify this theoretically calculated amount of utilizable O2, these results suggest that the tissue oxygenation efficacy of hyperoxic ventilation, even in absence of hypoxemia, is grossly underestimated in daily clinical practice.
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Introduction: The pathophysiological basis of neurological decompression sickness and the association between cerebral subcortical white matter (WM) change and nonhypoxic hypobaria remain poorly understood. Recent study of altitude decompression sickness risk evaluated acute WM responses to intensive hypobaric exposure using brain magnetic resonance imaging.
Methods: Six healthy men (20 to 50 yr) completed 6 h of hyperoxic hypobaria during three same-day altitude chamber decompressions to pressure altitudes ≥ 22,000 ft (6706 m).
Biomedicines
March 2024
Department of Pediatrics, Graduate School of Medicine, Akita University, Akita 010-8543, Japan.
Background: Pyruvate dehydrogenase kinase isoform 4 (PDK4) plays a pivotal role in the regulation of cellular proliferation and apoptosis. The objective of this study was to examine whether the genetic depletion of the PDK4 gene attenuates hyperoxia-induced lung injury in neonatal mice.
Methods: Neonatal PDK4-/- mice and wild-type (WT) mice were exposed to oxygen concentrations of 21% (normoxia) and 95% (hyperoxia) for the first 4 days of life.
Cureus
March 2024
Ophthalmology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education and Research, Wardha, IND.
Retinopathy of prematurity (ROP) is a rare proliferative ocular condition that can happen in premature babies (born preterm <36 weeks) or who weigh <1.5 kg at birth (low birth weight babies). ROP is a major cause of childhood blindness.
View Article and Find Full Text PDFFree Radic Biol Med
February 2024
Department of Pediatrics, Division of Neonatal-Perinatal Medicine, Baylor College of Medicine, Texas Children's Hospital, Houston, TX, United States. Electronic address:
Pregnant women exposed to polycyclic aromatic hydrocarbons (PAHs) are at increased risk for premature delivery. Premature infants often require supplemental oxygen, a known risk factor for bronchopulmonary dysplasia (BPD). Cytochrome P450 (CYP) enzymes have been implicated in hyperoxic lung injury.
View Article and Find Full Text PDFPediatr Res
January 2024
Division of Neonatology, Department of Pediatrics, University of Washington, Seattle, WA, USA.
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