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Background: Anemia is common among hospitalized critically ill and surgical oncological patients. The rising incidence of cancer and aggressive treatments has increased the demand for blood products, further strained by a dwindling donor pool. The normobaric oxygen paradox (NOP) has emerged as a potential avenue to increase EPO levels. While some studies support its efficacy, research remains limited in clinical settings. This study aims to assess the effectiveness of a NOP protocol in stimulating erythropoiesis, as measured by changes in reticulocyte counts, in cancer patients undergoing abdominal surgeries. Methods: This is a post hoc analysis of a prospective, single-center, controlled, randomized study. A total of 49 patients undergoing abdominal surgery were analyzed at the Institut Jules Bordet. Adult patients admitted to the intensive care unit (ICU) for at least 24 h were enrolled, excluding those with severe renal insufficiency or who received transfusions during the study period. Participants were randomized into two groups: a normobaric oxygen paradox (OXY) group who received 60% oxygen for 2 h on days 1, 3, and 5 post-surgery and a control (CTR) group who received standard care. Data on baseline characteristics, surgical details, and laboratory parameters were collected. Statistical analysis included descriptive statistics, chi-square tests, t-tests, Mann–Whitney tests, and linear and logistic regression. Results: The final analysis included 33 patients (median age 62 [IQR 58–66], 28 (84.8%) males, with no withdrawals or deaths during the study period. No significant differences were observed in baseline surgical characteristics or perioperative outcomes between the two groups. In the OXY group (n = 16), there was a significant rise (p = 0.0237) in the percentage of reticulocyte levels in comparison to the CTR group (n = 17), with median values of 36.1% (IQR 20.3–57.8) versus − 5.3% (IQR − 19.2–57.8), respectively. The increases in hemoglobin and hematocrit levels did not significantly differ between the groups when compared to their baselines’ values. Conclusions: This study provides preliminary evidence supporting the potential of normobaric oxygen therapy in stimulating erythropoiesis in cancer patients undergoing abdominal surgeries. While the OXY group resulted in increased reticulocyte counts, further research with larger sample sizes and multi-center trials is warranted to confirm these findings. Trial registration: The study was retrospectively registered under NCT number 06321874 on The 10th of April 2024. [ABSTRACT FROM AUTHOR]

Background: Chemoresistance is a substantial obstacle in cancer therapy. The microenvironment of solid tumor growth can be hypoxic, which promotes the survival, growth, and progression of cancer cells and reduces the effects of chemotherapy and radiotherapy. Hyperoxia treatment has potential to enhance cancer therapies. Objective: We evaluated whether normobaric hyperoxia (NBO) therapy has an anticancer effect and can be a strategy for overcoming anticancer drug resistance. Human alveolar adenocarcinoma (A549) and paclitaxel (PTX)-resistant (A549/PR) cell lines were used. Cells were assessed after exposure to room air (RA) or NBO for 48 h with and without PTX application. Results: NBO exposure inhibited cell viability, migration abilities, and proliferation in both cell lines. Chemo-resistant cell lines have shown variable viability upon NBO exposure. NBO exposure induced critical cytotoxicity and attenuated the characteristics of cancer in A549/PR cells. NBO induced a decline of chemoresistance in A549/PR cells when co-treated with PTX, consequently increasing cell death. In addition, NBO leads to intracellular reactive oxygen species and induced endoplasmic reticulum (ER) stress through the CCAAT/enhancer-binding protein homologous protein (CHOP) signaling pathway. Conclusion: In summary, NBO increased cell death in lung cancer cells and promoted PTX re-sensitization in A549/PR cells through apoptosis and CHOP-mediated ER stress. [ABSTRACT FROM AUTHOR]

Purpose: We investigated the effects of a relatively inexpensive, non-invasive, short-term treatment with low-dose normobaric hyperoxia (NBH) on macular edema in patients with retinal vein occlusion (RVO). Methods: Participants with macular edema associated with RVO were treated with 5 LPM of NBH via facemask (40% fraction of inspired oxygen, FIO2) for 3 h. Patients with non-fovea involving edema who elected to be observed returned for a second treatment 1 month later to test reproducibility. Results: A 3-h session of NBH (n = 45) resulted in decreased maximum macular thickness (MMT) (mean 7.10%, t34=9.63 P<.001) and central macular thickness (CMT) (mean 4.64%, t34=6.90, P<.001) when compared to untreated eyes with RVO measured over the same period of time (n = 12) or their healthy fellow eye (n = 34; MMT:t34=−9.60, P<.001;CMT: t34=−6.72, P<.001). Patients who had a second NBH treatment 1 month later experienced a recurrence of their edema, but demonstrated a similar significant reduction in MMT and CMT after the second NBH treatment. Conclusions: Three-hour treatment with 40% FIO2 NBH results in a significant reduction in MMT and CMT. This study supports an ischemic mechanism for macular edema associated with retinal vein occlusion. Translational relevance: Short-term low-dose normobaric hyperoxia is a simple, inexpensive, and ubiquitous treatment that may provide an alternate or adjunctive approach to treating macular edema in patients who are resistant to or cannot afford anti-VEGF medications. [ABSTRACT FROM AUTHOR]

Blast-induced traumatic brain injury (bTBI) is a leading cause of disability and mortality in soldiers during the conflicts in Iraq and Afghanistan. Although substantial clinical and animal studies have investigated the pathophysiology and treatments of bTBI, few effective therapies have been found, especially for the early rescue in the battlefield. The aim of this study is to evaluate neuroprotective effects of early normobaric hyperoxia (NBO) on bTBI. We established a rat model of bTBI caused by explosion in the cabin. It exhibited typical changes of mild bTBI, like impaired neurological function, brain edema, minor intracranial hemorrhage and neuron necrosis. The rats were divided into 4 groups (n = 12): Sham, Vehicle, hyperbaric oxygen (HBO) and NBO. Neurological function of the rats was assessed by the Neurological Severity Scores (NSS) at 24 h and 72 h after explosion. Serum interleukin-6 (IL-6), neuron specific enolase (NSE) and tau protein were measured at 24 h and 72 h after explosion. Brain water content was measured and Aquaporin-4 (AQP4) immunostaining was performed. Neuronal apoptosis was analyzed by TUNEL staining. NBO demonstrated curative effects on protecting the neurological function. Serum levels of NSE and tau protein were reduced at 24 h and 72 h after explosion. But the levels of IL-6 were not reduced significantly at both time points. Cerebral edema was alleviated. Simultaneously, AQP4 immunostaining of the hippocampus showed remarkably decreased expression after treatment. The number of apoptotic cells in hippocampus was also decreased. Compared with HBO, NBO is simple and convenient, and can be administered in remote areas. It may be a promising therapy for early rescue of bTBI in the battlefield. [ABSTRACT FROM AUTHOR]

Abstract—A hypothesis about the mechanism of radiosensitizing effect of hyperoxia during irradiation on the course and outcome of gastrointestinal radiation syndrome in the absence of significant modification of the course of hematopoietic radiation syndrome is presented. The important role of an increased production of reactive oxygen species (ROS) in hyperoxia in promoting gastrointestinal radiation injury in the absence of a significant contribution of the "oxygen effect" to this process is considered. The role of the accumulation of the toxic effects of ROS under repeated hyperoxia with exposure to fractionated irradiation in exacerbating acute radiation syndrome is emphasized. Attention is paid to the role of the preliminary daily stress effect of vibration on the potentiation of the radiosensitizing effect of hyperoxia on the course of gastrointestinal radiation syndrome. The metabolic changes in the regulation of the energy supply of the body under combined exposure to ionizing radiation and hyperoxia are analyzed. Possible mechanisms of radiomitigating effect of hyperoxia on the hematopoietic tissue, manifested during short-term 100% oxygen breathing before or immediately after irradiation of animals are considered. The signaling role of ROS and the cytostatic effect caused by hyperoxia in enhancing the postradiation recovery of hemopoietic tissue is emphasized. [ABSTRACT FROM AUTHOR]

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An inspiratory oxygen fraction of 1.0 is often required to avoid hypoxia both in many pre- and in-hospital situations. On the other hand, hyperoxia may lead to deleterious consequences (cell growth inhibition, inflammation, and apoptosis) for numerous tissues including the lung. Whereas clinical effects of hyperoxic lung injury are well known, its impact on the expression of lung proteins has not yet been evaluated sufficiently. The aim of this study was to analyze time-dependent alterations of protein expression in rat lung tissue after short-term normobaric hyperoxia (NH). After approval of the local ethics committee for animal research, N = 36 Wistar rats were randomized into six different groups: three groups with NH with exposure to 100 % oxygen for 3 h and three groups with normobaric normoxia (NN) with exposure to room air (21 % oxygen). After the end of the experiments, lungs were removed immediately (NH and NN), after 3 days (NH and NN) and after 7 days (NH and NN). Lung lysates were analyzed by two-dimensional gel electrophoresis (2D-GE) followed by peptide mass fingerprinting using mass spectrometry. Statistical analysis was performed with Delta 2D (DECODON GmbH, Greifswald, Germany; ANOVA, Bonferroni correction, p < 0.01). Biological functions of differential regulated proteins were studied using functional network analysis (Ingenuity Pathways Analysis, IPA). pO was significantly higher in NH-groups compared to NN-groups (581 ± 28 vs. 98 ± 12 mmHg; p < 0.01), all other physiological parameters did not differ. Expression of 14 proteins were significantly altered: two proteins were up-regulated and 12 proteins were down-regulated. Even though NH was comparatively short termed, significant alterations in lung protein expression could be demonstrated up to 7 days after hyperoxia. The identified proteins indicate an association with cell growth inhibition, regulation of apoptosis, and approval of structural cell integrity. [ABSTRACT FROM AUTHOR]

The development of cerebral vasoconstriction in subarachnoid hemorrhage (SAH) induced by the rupture of an aneurism of brain vessels impairs cerebral circulation. Treatment with normobaric hyperoxia may be used as an effective approach to oxygen delivery to the injured brain tissue. The purpose of the present study was to evaluate the effects of normobaric hyperoxia on oxidative stress and factors of endogenous vascular regulation in eight patients who suffered from non-traumatic SAH and remained in critical condition. The intensity of oxidative stress was assayed by measuring malonic dialdehyde and the total antioxidant activity in the blood serum. Endothelium functions were evaluated using the content of the stable metabolites of nitric oxide and the activity of angiotensin-converting enzyme in the blood serum. The data from eight patients who suffered from non-traumatic SAH showed an enhancement of oxidative stress, which influenced the functions of the vascular endothelium and resulted in an imbalance in the endogenous regulation of vascular tone. Treatment with normobaric hyperoxia was not associated with intensification of free-radical processes in patients who suffered from non-traumatic SAH and did not influence intracranial and arterial pressure. [ABSTRACT FROM AUTHOR]

Sufficient oxygenation is indispensable for cognitive performance in mammals. In order to assure adequate oxygenation and to prevent hypoxia in medicine or aviation, different approaches of oxygen delivery are realized. With regard to hyperoxia, it is well known that it increases the risk of tissue toxicity and inflammation by generating radical oxygen species. However, this impact of hyperoxia on the expression of specific brain proteins has not been evaluated in detail yet. The present study analyzes time-dependent changes in protein expression in rat brain after a short-term exposure to normobaric hyperoxia. Thirty-six Wistar rats were randomly assigned to six different groups, three normobaric hyperoxia (NH) groups or three normobaric normoxia (NN) groups, each consisting of n = 6 animals. NH animals were exposed to 100% oxygen, NN rats to 21% oxygen, each group for 3 h. One group of NH and one group of NN were killed immediately after the 3 h, one group each after 3 days and one group each after 7 days. Rat brains were removed for analysis and whole brain detergent protein lysates were separated via two-dimensional gel electrophoresis followed by subsequent identification of protein expression alterations by peptide mass fingerprinting using mass spectrometry. Also, a functional network mapping and molecular pathway analysis were carried out. Statistical analysis was performed using analysis of variance (ANOVA) with Bonferroni correction using P < 0.01. Physiological parameters of the animals did not differ significantly between the two groups except for partial oxygen pressure (580 vs. 89 mmHg; P < 0.05). The expression of nine proteins was found to be significantly altered (five up-regulated: GOT1, CCT2, TCP1, G6PD, and ALB; four down-regulated: PEBP1, PRDX2, ENO1, and MDH1). IPA generated a network with eight focus proteins associated with pathways in “cell death, cancer, and signalling”. Although hyperoxia was normobaric and induced for only 3 h, significant changes in brain protein expression were detectable immediately after the 3 h, after 3 days, as well as after 7 days. This may indicate effects on brain protein expression take place in the rat brain following a relatively short period of hyperoxia. [ABSTRACT FROM AUTHOR]

This study focuses on the effect of hyperoxia on maximal oxygen uptake $$ {\left( {\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2\max }} } \right)} $$ and maximal power ( Pmax) in subjects exhibiting exercise-induced arterial hypoxemia (EIH) at sea level. Sixteen competing male cyclists $$ \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2\max }} $$>60 ml·min−1·kg−1) performed exhaustive ramp exercise (cycle-ergometer) under normoxia and moderate hyperoxia (FIO2=30%). After the normoxic trial, the subjects were divided into those demonstrating EIH during exercise [arterial O2 desaturation (Δ SaO2) >5%; n=9] and those who did not ( n=7). Under hyperoxia, SaO2 raised and the increase was greater for the EIH than for the non-EIH group ( P<0.001). $$ \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2\max }} $$ improved for both groups and to a greater extent for EIH (12.8±5.7% vs. 4.2±4.6%, P<0.01; mean±SD) and the increase was correlated to the gain in SaO2 for all subjects ( r=0.71, P<0.01). Pmax improved by 3.3±3.3% ( P<0.01) regardless of the group. These data suggest that pulmonary gas exchange contributes to a limitation in $$ \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2\max }} $$ and power for especially EIH subjects. [ABSTRACT FROM AUTHOR]

Few studies evidenced an enhancement in oxygen uptakeduring submaximal exercise in hyperoxia. This O2 “overconsumption” seems to increase above the lactate threshold. The aim of this study was to determine whether the hyperoxia-induced enhancement inmay be related to a higher metabolism of lactate. Nine healthy males (aged 23.1 years, mean= 53.8 ml min-1 kg-1) were randomized to two series of exercise in either normoxia or hyperoxia corresponding to an inspired O2 fraction (FIO2) of 30%. Each series consisted of 6 min cycling at 50%(Moderate1), 5 min cycling at 95%(Near Max) and then 6 min at 50%(Moderate2). In both series Near Max was performed in normoxia.was significantly greater under hyperoxia than in normoxia during Moderate1 (2192±189 vs. 2025±172 ml min-1) and during Moderate2 (2352±173 vs. 2180±193 ml min-1). However, the effect of the high FIO2 was not significantly different on(+172±137 ml min-1 with [La] ~ 6 mmol l-1) compared to(+166±133 ml min-1 with [La] ~ 2.4 mmol l-1). [La] at the onset of Moderate2 was not different between normoxia and hyperoxia (10.1±2.2 vs. 10.9±1.6 mmol l-1). The results show thatis significantly increased during moderate exercise in hyperoxia. But this O2 overconsumption was not modified by a high [La] induced by a prior heavy exercise. It could be concluded that lactate accumulation is not directly responsible for the increase in O2 overconsumption with intensity during exercise in hyperoxia. [ABSTRACT FROM AUTHOR]

The present study examined the effect of hyperoxia on oxygen uptake (VO2) and on maximal oxygen uptake (VO2max) during incremental exercise (IE) and constant work rate exercise (CWRE). Ten subjects performed IE on a bicycle ergometer under normoxic and hyperoxic conditions (30% oxygen). They also performed four 12-min bouts of CWRE at 40, 55, 70 and 85% of normoxic VO2max (ex1, ex2, ex3 and ex4, respectively) in normoxia and in hyperoxia. VO2max was significantly improved by 15.0 (15.2)% under hyperoxia, while performance (maximum workload, Wmax) was improved by only +4.5 (3.0)%. During IE, the slope of the linear regression relating VO2 to work rate was significantly steeper in hyperoxia than in normoxia [10.80 (0.88) vs 10.06 (0.66) ml·min–1·W–1]. During CWRE, we found a higher VO2 at ex1, ex2, ex3 and ex4, and a higher VO2 slow component at ex4 under hyperoxia. We have shown that breathing hyperoxic gas increases VO2max, but to an extent that is difficult to explain by an increase in oxygen supply alone. Changes in metabolic response, fibre type recruitment and VO2 of non-exercising tissue could explain the additional VO2 for a given submaximal work rate under hyperoxia. [ABSTRACT FROM AUTHOR]

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