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Thematische Bibliographien / Normobaric oxygen paradox (NOP) / Zeitschriftenartikel

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Zeitschriftenartikel zum Thema „Normobaric oxygen paradox (NOP)“

Autor: Grafiati

Veröffentlicht am 16. November 2024

Zuletzt aktualisiert am 19. Juli 2025

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1

Lafère, Pierre, Thomas Schubert, David De Bels, Peter Germonpré, and Costantino Balestra. "Can the normobaric oxygen paradox (NOP) increase reticulocyte count after traumatic hip surgery?" Journal of Clinical Anesthesia 25, no. 2 (2013): 129–34. http://dx.doi.org/10.1016/j.jclinane.2012.06.021.

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2

Fratantonio, Deborah, Fabio Virgili, Alessandro Zucchi, et al. "Increasing Oxygen Partial Pressures Induce a Distinct Transcriptional Response in Human PBMC: A Pilot Study on the “Normobaric Oxygen Paradox”." International Journal of Molecular Sciences 22, no. 1 (2021): 458. http://dx.doi.org/10.3390/ijms22010458.

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The term “normobaric oxygen paradox” (NOP), describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as oxygen shortage, and resulting in up-regulation of the Hypoxia-inducible factor 1α (HIF-1α) transcription factor activity. The molecular characteristics of this response have not been yet fully characterized. Herein, we report the activation time trend of oxygen-sensitive transcription factors in human peripheral blood mononuclear cells (PBMCs) obtained from healthy subjects after one hour of exposure to mild (MH), high (HH) and very high (VHH) hyperoxia, corresponding to 30%, 100%, 140% O2, respectively. Our observations confirm that MH is perceived as a hypoxic stress, characterized by the activation of HIF-1α and Nuclear factor (erythroid-derived 2)-like 2 (NRF2), but not Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB). Conversely, HH is associated to a progressive loss of NOP response and to an increase in oxidative stress leading to NRF2 and NF-kB activation, accompanied by the synthesis of glutathione (GSH). After VHH, HIF-1α activation is totally absent and oxidative stress response, accompanied by NF-κB activation, is prevalent. Intracellular GSH and Matrix metallopeptidase 9 (MMP-9) plasma levels parallel the transcription factors activation pattern and remain elevated throughout the observation time. In conclusion, our study confirms that, in vivo, the return to normoxia after MH is sensed as a hypoxic trigger characterized by HIF-1α activation. On the contrary, HH and VHH induce a shift toward an oxidative stress response, characterized by NRF2 and NF-κB activation in the first 24 h post exposure.

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Balestra, Costantino, Sara Baldelli, Fabio Virgili, Michele Salvagno, Simona Mrakic-Sposta, and Deborah Fratantonio. "Pulsed Hyperoxia Acts on Plasmatic Advanced Glycation End Products and Advanced Oxidation Protein Products and Modulates Mitochondrial Biogenesis in Human Peripheral Blood Mononuclear Cells: A Pilot Study on the “Normobaric Oxygen Paradox”." International Journal of Molecular Sciences 25, no. 4 (2024): 2394. http://dx.doi.org/10.3390/ijms25042394.

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The “normobaric oxygen paradox” (NOP) describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as an oxygen shortage, up-regulating redox-sensitive transcription factors. We have previously characterized the time trend of oxygen-sensitive transcription factors in human PBMCs, in which the return to normoxia after 30% oxygen is sensed as a hypoxic trigger, characterized by hypoxia-induced factor (HIF-1) activation. On the contrary, 100% and 140% oxygen induce a shift toward an oxidative stress response, characterized by NRF2 and NF-kB activation in the first 24 h post exposure. Herein, we investigate whether this paradigm triggers Advanced Glycation End products (AGEs) and Advanced Oxidation Protein Products (AOPPs) as circulating biomarkers of oxidative stress. Secondly, we studied if mitochondrial biogenesis was involved to link the cellular response to oxidative stress in human PBMCs. Our results show that AGEs and AOPPs increase in a different manner according to oxygen dose. Mitochondrial levels of peroxiredoxin (PRX3) supported the cellular response to oxidative stress and increased at 24 h after mild hyperoxia, MH (30% O2), and high hyperoxia, HH (100% O2), while during very high hyperoxia, VHH (140% O2), the activation was significantly high only at 3 h after oxygen exposure. Mitochondrial biogenesis was activated through nuclear translocation of PGC-1α in all the experimental conditions. However, the consequent release of nuclear Mitochondrial Transcription Factor A (TFAM) was observed only after MH exposure. Conversely, HH and VHH are associated with a progressive loss of NOP response in the ability to induce TFAM expression despite a nuclear translocation of PGC-1α also occurring in these conditions. This study confirms that pulsed high oxygen treatment elicits specific cellular responses, according to its partial pressure and time of administration, and further emphasizes the importance of targeting the use of oxygen to activate specific effects on the whole organism.

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Balestra, Costantino, Kate Lambrechts, Simona Mrakic-Sposta, et al. "Hypoxic and Hyperoxic Breathing as a Complement to Low-Intensity Physical Exercise Programs: A Proof-of-Principle Study." International Journal of Molecular Sciences 22, no. 17 (2021): 9600. http://dx.doi.org/10.3390/ijms22179600.

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Inflammation is an adaptive response to both external and internal stimuli including infection, trauma, surgery, ischemia-reperfusion, or malignancy. A number of studies indicate that physical activity is an effective means of reducing acute systemic and low-level inflammation occurring in different pathological conditions and in the recovery phase after disease. As a proof-of-principle, we hypothesized that low-intensity workout performed under modified oxygen supply would elicit a “metabolic exercise” inducing a hormetic response, increasing the metabolic load and oxidative stress with the same overall effect expected after a higher intensity or charge exercise. Herein, we report the effect of a 5-week low-intensity, non-training, exercise program in a group of young healthy subjects in combination with the exposure to hyperoxia (30% and 100% pO2, respectively) or light hypoxia (15% pO2) during workout sessions on several inflammation and oxidative stress parameters, namely hemoglobin (Hb), redox state, nitric oxide metabolite (NOx), inducible nitric oxide synthase (iNOS), inflammatory cytokine expression (TNF-α, interleukin (IL)-6, IL-10), and renal functional biomarkers (creatinine, neopterin, and urates). We confirmed our previous reports demonstrating that intermittent hyperoxia induces the normobaric oxygen paradox (NOP), a response overlapping the exposure to hypoxia. Our data also suggest that the administration of modified air composition is an expedient complement to a light physical exercise program to achieve a significant modulation of inflammatory and immune parameters, including cytokines expression, iNOS activity, and oxidative stress parameters. This strategy can be of pivotal interest in all those conditions characterized by the inability to achieve a sufficient workload intensity, such as severe cardiovascular alterations and articular injuries failing to effectively gain a significant improvement of physical capacity.

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Debevec, Tadej, Michail E. Keramidas, Barbara Norman, Thomas Gustafsson, Ola Eiken, and Igor B. Mekjavic. "No Evidence For The "Normobaric Oxygen Paradox"." Medicine & Science in Sports & Exercise 43, Suppl 1 (2011): 151. http://dx.doi.org/10.1249/01.mss.0000403127.23300.30.

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6

Balestra, Costantino, Peter Germonpré, Jacques R. Poortmans, and Alessandro Marroni. "Serum erythropoietin levels in healthy humans after a short period of normobaric and hyperbaric oxygen breathing: the “normobaric oxygen paradox”." Journal of Applied Physiology 100, no. 2 (2006): 512–18. http://dx.doi.org/10.1152/japplphysiol.00964.2005.

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Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24–36 h. A 60% increase ( P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the “normobaric oxygen paradox,” does not appear to be present after hyperbaric oxygen breathing.

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Salvagno, Michele, Giacomo Coppalini, Fabio Silvio Taccone, et al. "The Normobaric Oxygen Paradox—Hyperoxic Hypoxic Paradox: A Novel Expedient Strategy in Hematopoiesis Clinical Issues." International Journal of Molecular Sciences 24, no. 1 (2022): 82. http://dx.doi.org/10.3390/ijms24010082.

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Hypoxia, even at non-lethal levels, is one of the most stressful events for all aerobic organisms as it significantly affects a wide spectrum of physiological functions and energy production. Aerobic organisms activate countless molecular responses directed to respond at cellular, tissue, organ, and whole-body levels to cope with oxygen shortage allowing survival, including enhanced neo-angiogenesis and systemic oxygen delivery. The benefits of hypoxia may be evoked without its detrimental consequences by exploiting the so-called normobaric oxygen paradox. The intermittent shift between hyperoxic-normoxic exposure, in addition to being safe and feasible, has been shown to enhance erythropoietin production and raise hemoglobin levels with numerous different potential applications in many fields of therapy as a new strategy for surgical preconditioning aimed at frail patients and prevention of postoperative anemia. This narrative review summarizes the physiological processes behind the proposed normobaric oxygen paradox, focusing on the latest scientific evidence and the potential applications for this strategy. Future possibilities for hyperoxic-normoxic exposure therapy include implementation as a synergistic strategy to improve a patient’s pre-surgical condition, a stimulating treatment in critically ill patients, preconditioning of athletes during physical preparation, and, in combination with surgery and conventional chemotherapy, to improve patients’ outcomes and quality of life.

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Keramidas, Michail E., Ola Eiken, and Igor B. Mekjavic. "Prevailing evidence contradicts the notion of a “normobaric oxygen paradox”." European Journal of Applied Physiology 112, no. 12 (2012): 4177–78. http://dx.doi.org/10.1007/s00421-012-2394-9.

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Balestra, C., and P. Germonpré. "Hypoxia, a multifaceted phenomenon: the example of the “Normobaric Oxygen Paradox”." European Journal of Applied Physiology 112, no. 12 (2012): 4173–75. http://dx.doi.org/10.1007/s00421-012-2392-y.

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Balestra, C., and P. Germonpré. "Increasing EPO using the normobaric oxygen paradox: a ‘not so simple’ task." Acta Physiologica 203, no. 2 (2011): 287–88. http://dx.doi.org/10.1111/j.1748-1716.2011.02282.x.

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Keramidas, M. E., S. N. Kounalakis, T. Debevec, et al. "Acute normobaric hyperoxia transiently attenuates plasma erythropoietin concentration in healthy males: evidence against the ‘normobaric oxygen paradox’ theory." Acta Physiologica 202, no. 1 (2011): 91–98. http://dx.doi.org/10.1111/j.1748-1716.2011.02262.x.

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De Bels, D., F. Corazza, P. Germonpré, and C. Balestra. "The normobaric oxygen paradox: A novel way to administer oxygen as an adjuvant treatment for cancer?" Medical Hypotheses 76, no. 4 (2011): 467–70. http://dx.doi.org/10.1016/j.mehy.2010.11.022.

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Ciccarella, Y., C. Balestra, J. Valsamis, and P. Van der Linden. "Increase in endogenous erythropoietin synthesis through the normobaric oxygen paradox in cardiac surgery patients." British Journal of Anaesthesia 106, no. 5 (2011): 752–53. http://dx.doi.org/10.1093/bja/aer074.

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Zuccari, S., A. Donati, E. Damiani, R. Castagnani, N. Mininno, and P. Pelaia. "Normobaric oxygen paradox and erythropoietin production in critically ill patients: a prospective observational study." Critical Care 19, Suppl 1 (2015): P320. http://dx.doi.org/10.1186/cc14400.

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Cimino, F., C. Balestra, P. Germonpré, et al. "Pulsed high oxygen induces a hypoxic-like response in human umbilical endothelial cells and in humans." Journal of Applied Physiology 113, no. 11 (2012): 1684–89. http://dx.doi.org/10.1152/japplphysiol.00922.2012.

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It has been proposed that relative changes of oxygen availability, rather than steady-state hypoxic or hyperoxic conditions, play an important role in hypoxia-inducible factor (HIF) transcriptional effects. According to this hypothesis describing the “normobaric oxygen paradox”, normoxia following a hyperoxic event is sensed by tissues as an oxygen shortage, upregulating HIF-1 activity. With the aim of confirming, at cellular and at functional level, that normoxia following a hyperoxic event is “interpreted” as a hypoxic event, we report a combination of experiments addressing the effects of an intermittent increase of oxygen concentration on HIF-1 levels and the activity level of specific oxygen-modulated proteins in cultured human umbilical vein endothelial cells and the effects of hemoglobin levels after intermittent breathing of normobaric high (100%) and low (15%) oxygen in vivo in humans. Our experiments confirm that, during recovery after hyperoxia, an increase of HIF expression occurs in human umbilical vein endothelial cells, associated with an increase of matrix metalloproteinases activity. These data suggest that endothelial cells “interpret” the return to normoxia after hyperoxia as a hypoxic stimulus. At functional level, our data show that breathing both 15 and 100% oxygen 30 min every other day for a period of 10 days induces an increase of hemoglobin levels in humans. This effect was enhanced after the cessation of the oxygen breathing. These results indicate that a sudden decrease in tissue oxygen tension after hyperoxia may act as a trigger for erythropoietin synthesis, thus corroborating the hypothesis that “relative” hypoxia is a potent stimulator of HIF-mediated gene expressions.

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Donati, A., E. Damiani, AT Colesnicenco, et al. "Normobaric oxygen paradox and the microcirculation in the critically ill patient: a prospective observational study." Critical Care 18, Suppl 1 (2014): P168. http://dx.doi.org/10.1186/cc13358.

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Busławski, Adam, Joachim Jarzyna, and Jerzy Zwoździak. "Biological mechanisms, therapeutic applications, clinical benefits and future perspectives of normobaric oxygen therapy: literature review." Medical Science Pulse 18, no. 4 (2024): 43–64. https://doi.org/10.5604/01.3001.0055.0364.

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Background: Normobaric oxygen therapy (NBO) is a widely used medical intervention aimed at enhancing oxygen delivery to tissues under atmospheric pressure. Recent studies have demonstrated its potential therapeutic benefits across various medical conditions, including stroke, traumatic brain injury, cardiovascular diseases, stress and mental disorders as well as wound healing.Aim of the study: This literature review aimed to summarize the biological mechanisms, therapeutic potential, and clinical outcomes of NBO exposures. Material and methods: A literature review was conducted, focusing on clinical trials, experimental studies, and narrative reviews discussing the biological mechanisms, therapeutic protocols, and outcomes. The search strategy focused on peer-reviewed and English-language publications from major medical and scientific databases, including PubMed, Scopus, Web of Science, and Embase, covering the period from 2010 to 2025 to ensure a comprehensive and evidence-based synthesis. Results: NBO exerts its therapeutic effects through multiple pathways, including enhanced oxygenation, stimulation of erythropoiesis via the normobaric oxygen paradox, modulation of inflammatory pathways, and improvement of mitochondrial function. Clinical evidence supports its application in neurological rehabilitation, cardiovascular conditions, wound healing, and respiratory support. However, despite its therapeutic potential, the standardization of treatment protocols, optimization of dosing regimens, and assessment of long-term safety remain critical research gaps requiring further investigation.Conclusions: NBO presents a promising, non-invasive therapeutic approach with broad clinical applications. However, further large-scale randomized controlled trials are necessary to establish standardized guidelines, optimize dosing protocols, and evaluate long-term safety. Future research should also explore the integration of NBO into precision medicine and rehabilitation strategies.

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Debevec, Tadej, Michail E. Keramidas, Barbara Norman, Thomas Gustafsson, Ola Eiken, and Igor B. Mekjavic. "Acute short-term hyperoxia followed by mild hypoxia does not increase EPO production: resolving the “normobaric oxygen paradox”." European Journal of Applied Physiology 112, no. 3 (2011): 1059–65. http://dx.doi.org/10.1007/s00421-011-2060-7.

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Perović, Antonija, Marko Žarak, Marina Njire Bratičević, and Jerka Dumić. "Effects of recreational scuba diving on erythropoiesis–“normobaric oxygen paradox” or “plasma volume regulation” as a trigger for erythropoietin?" European Journal of Applied Physiology 120, no. 7 (2020): 1689–97. http://dx.doi.org/10.1007/s00421-020-04395-5.

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BALESTRA, COSTANTINO, PETER GERMONPRÉ, PIERRE LAFERE, YANNICK CICCARELLA, and PHILIPPE VAN DER LINDEN. "The ‘normobaric oxygen paradox’: a simple way to induce endogenous erythropoietin production and concomitantly raise hemoglobin levels in anemic patients." Transfusion Alternatives in Transfusion Medicine 11, no. 1 (2010): 39–42. http://dx.doi.org/10.1111/j.1778-428x.2010.01127.x.

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Ricerca, Bianca Maria, Salvatore Vagnoni, Anna Maria D’Amore, et al. "Erythropoietin Production in Vivo after a Fourteen Days Exposition to Hyperbarism." Blood 112, no. 11 (2008): 5398. http://dx.doi.org/10.1182/blood.v112.11.5398.5398.

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Abstract Six Italian scuba divers, three men and three women, lived permanently for 14 days at a depth of 8 – 10 metres under the sea level breathing a mixture with the same composition of the air at a pressure ranging between 1,8–2 ATA (Hyperoxic Air-HOA), under the control of a physician’s team. This experience called Abyss project: the “underwater home” was born as a Guinness record attempt, but it had been also surrounded by scientific attention giving the opportunity to collect scientific data. The effect of long-term diving on blood in professional and recreational-professional scuba divers has not been studied. Oxygen is the main regulator of Epo production through the activation or degradation of HIF-1α, the most important transcriptional factor of Epo gene. Hypoxia favours HIF-1α activation, on the contrary hyperoxia favours its degradation. In this case, the excess of Reactive Oxygen Species (ROS), play a crucial role. In the six subjects of Abyss Project, we evaluated S-Epo (Immunoturbidimetric method-Immulite Medical System), CBC and differential (ADVIA 120 Automated Hematology System-Bayer Diagnostics), Reticulocyte count (absolute and perceptual) (Beckman Coulter LH 750-IL Instruments).and the most important hemato-chemical parameters with this timing: before immersion (TIME 0), 7 days (TIME 1), 14 days (TIME 2) after beginning the dive, two hours (TIME 3) and 24 hours (TIME 4) after the resurface. The aim of our study was to investigate if erythropoiesis is affected by a so long diving. Hgb, as far as the hematochemical parameters did not change while Ht, s-Epo, O/P ratio absolute and perceptual reticulocyte counts decline progressively from TIME 0 until TIME 3. At Time 4 (24 hours after the resurface) a rise of Epo production was observed. No significant variation of renal function was registered, According to Repeated Measures ANOVA test, these results are statistically significant (see the Table). We retain that the different results of Hgb and Ht reflect a variation of hydration state. Similar results were obtained previously by other Authors (Balestra C et al J Appl Physiol 2006) although in different experimental conditions and for shorter exposition. Their experiment was conducted in two steps: hyperoxia (100% O2, two hours, with a “nonrebreather” mask) in normobarysm; hyperoxia in hyperbarysm (100% O2, 2,5 ATA, 1,5 hours, in hyperbaric chamber). They observed the rise of s-Epo only 24 hours after the exposition to normobarism, not after the exposition to hyperbarism. This phenomenon was called “normobaric oxygen paradox”. Our results confirm that the s-Epo production is affected by the exposition to hyperbarism. It could be hypothesize that the Oxygen dissolved in the plasma influences the s-Epo production, moving the equilibrium between reduction and oxidation towards the last. In fact, no relevant variation of the Hgb Oxygen transport was observed. The reverse of this equilibrium should determine the rise of s-Epo 24 hours after the resurface. Taking in account our results and those of Balestra, it seem that Oxygen pressure, more than O2 concentration, is crucial for the “normobaric oxygen paradox”. Finally, although Hgb did not change, some signs of impairment of erythropoiesis are already present. In fact, absolute and perceptual reticulocyte counts decline from Time 0 to time 4. Taking into account the timing of erythropoiesis, it is predictable that anemia would be a clinical problem if the exposition continued. In fact, erythropoiesis could suffer from the Epo reduction and also from the enhancement of the apoptosis. The last effect could be produced either by the Epo reduction, either by a direct effect of hyperoxia as demonstrated in vitro (Ganguly BJ Apoptosis 2002). T Hgb g/dl Ht Ret% Ret 10^9/l s-Epo mU/ml 0 14,03±1,25 41,32±2,81 1,19±0,35 56,40±22,09 11,58±3,09 1 13,72±1,39 40,03±3,37 1,08±0,50 50,72±26,16 6,28±3,20 2 13,33±1,80 38,83±4,35 0,72±0,23 32,58±12,82 4,23±1,59 3 13,40±1,43 39,77±3,38 0,67±0,17 30,18±8,90 4,50±1,73 4 13,67±1,35 39,82±3,43 0,71±0,28 32,96±13,44 14,02±5.05 P n.s. &lt;0.0001 &lt;0.0001 &lt;0.0001 &lt;0.0001

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Khalife, Maher, Michele Salvagno, Maurice Sosnowski, and Costantino Balestra. "Exploring the effects of post operative hyperoxic intermittent stimuli on reticulocyte levels in cancer patients: a randomized controlled study." Journal of Anesthesia, Analgesia and Critical Care 4, no. 1 (2024). http://dx.doi.org/10.1186/s44158-024-00179-x.

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Abstract 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.

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Khalife, Maher, Mohammed Ben Aziz, Costantino Balestra, Joseph Valsamis, and Maurice Sosnowski. "Physiological and Clinical Impact of Repeated Inhaled Oxygen Variation on Erythropoietin Levels in Patients After Surgery." Frontiers in Physiology 12 (September 27, 2021). http://dx.doi.org/10.3389/fphys.2021.744074.

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The “Normobaric Oxygen Paradox” (NOP) is a physiologic mechanism that induces an increase of endogenous erythropoietin (EPO) production by creating a state of relative hypoxia in subjects previously exposed to hyperoxia, followed by a rapid return to normoxia. Oxygen exposure duration and inspired oxygen fraction required to observe a significant increase in EPO or hemoglobin are not clearly defined. Consequently, we here study the effect of one model of relative hypoxia on EPO, reticulocytes and hemoglobin stimulation in patients after surgery. Patients were prospectively randomized in two groups. The O2 group (n = 10) received 100% oxygen for 1 h per day for eight consecutive days, via a non-rebreathing mask. The control group (n = 12) received no oxygen variation. Serum EPO, hemoglobin and reticulocyte count were measured on admission and postoperatively on days seven and nine. Percentage EPO at day nine with respect to the baseline value was significantly elevated within the groups [O2 group: 323.7 (SD ± 139.0); control group: 365.6 (SD± 162.0)] but not between them. No significant difference was found between the groups in terms of reticulocytes count and hemoglobin. Our NOP model showed no difference on EPO increase between the two groups. However, both groups expressed separately significant EPO elevation.

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Theunissen, S., D. De Bels, J. Devriendt, et al. "The normobaric oxygen paradox: does it increase haemoglobin?" Critical Care 15, S1 (2011). http://dx.doi.org/10.1186/cc9842.

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Van Meter, Keith W. "Hyperbaric oxygen therapy in the ATLS/ACLS resuscitative management of acutely ill or severely injured patients with severe anemia: a review." Frontiers in Medicine 11 (October 8, 2024). http://dx.doi.org/10.3389/fmed.2024.1408816.

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For short periods, even without the presence of red blood cells, hyperbaric oxygen can safely allow plasma to meet the oxygen delivery requirements of a human at rest. By this means, hyperbaric oxygen, in special instances, may be used as a bridge to lessen blood transfusion requirements. Hyperbaric oxygen, applied intermittently, can readily avert oxygen toxicity while meeting the body's oxygen requirements. In acute injury or illness, accumulated oxygen debt is shadowed by adenosine triphosphate debt. Hyperbaric oxygen efficiently provides superior diffusion distances of oxygen in tissue compared to those provided by breathing normobaric oxygen. Intermittent application of hyperbaric oxygen can resupply adenosine triphosphate for energy for gene expression and reparative and anti-inflammatory cellular function. This advantageous effect is termed the hyperbaric oxygen paradox. Similarly, the normobaric oxygen paradox has been used to elicit erythropoietin expression. Referfusion injury after an ischemic insult can be ameliorated by hyperbaric oxygen administration. Oxygen toxicity can be averted by short hyperbaric oxygen exposure times with air breaks during treatments and also by lengthening the time between hyperbaric oxygen sessions as the treatment advances. Hyperbaric chambers can be assembled to provide everything available to a patient in modern-day intensive care units. The complication rate of hyperbaric oxygen therapy is very low. Accordingly, hyperbaric oxygen, when safely available in hospital settings, should be considered as an adjunct for the management of critically injured or ill patients with disabling anemia.

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Ciccarella, Yannnick. "Increase of endogenous erythropoietin synthesis through the Normobaric Oxygen Paradox in cardiac surgery patients." BJA: British Journal of Anaesthesia 107, eLetters (2011). http://dx.doi.org/10.1093/bja/el_7094.

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Huggard, Joshua D., Nasimi A. Guluzade, James Duffin, and Daniel A. Keir. "The ventilatory response to modified rebreathing is unchanged by hyperoxic severity: implications for the hyperoxic hyperventilation paradox." Journal of Applied Physiology, November 9, 2023. http://dx.doi.org/10.1152/japplphysiol.00455.2023.

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Normobaric hyperoxia stimulates ventilation (V̇E) in a time- and dose-dependent manner. Whether this occurs via an oxygen (O2)-specific mechanism or secondary to carbon dioxide (CO2) retention at the central chemoreceptors remains unclear. We measured the ventilatory response to hyperoxic CO2 rebreathing with O2 clamped at increasingly higher pressures. We hypothesized that the V̇E versus PCO2 relationship is fixed and independent of PO2. On four occasions, twenty participants (10F; mean±SD age: 24±4 years) performed three repetitions of modified rebreathing in 4, randomized, isoxic-hyperoxic conditions: mild: PO2=150 mmHg; moderate: PO2=200 mmHg; high: PO2=300 mmHg; and extreme: PO2≈700 mmHg. Breath-by-breath V̇E, end-tidal CO2 (PETCO2) and O2 (PETO2) were measured by pneumotach and gas analyzer. For each rebreathing trial, the PETCO2 at which V̇E rose was identified as the ventilatory recruitment threshold (VRT, mmHg), data before VRT provided baseline V̇E (V̇EBSL, L∙min-1) and the slope of the response above VRT gave central chemoreflex sensitivity (V̇ES, L∙min-1∙mmHg-1). For each condition, VRT, V̇EBSL, and V̇ES from like-trials were averaged and repeated measures ANOVA assessed between-condition differences. There were no effects of PETO2 on V̇EBSL (mild: 7.4±4.2 L∙min-1; moderate: 6.9±4.2 L∙min-1; high: 6.5±3.7 L∙min-1; extreme: 7.5±2.7 L∙min-1; p=0.24), VRT (mild: 42.8±3.2 mmHg; moderate: 42.5±2.7 mmHg; high: 42.3±2.7 mmHg; extreme: 41.8±2.7 mmHg; p=0.07), or V̇ES (mild: 4.88±2.6 L∙min-1∙mmHg-1; moderate: 4.76±2.2 L∙min-1∙mmHg-1; high: 4.81±2.3 L∙min-1∙mmHg-1; extreme: 4.39±1.9 L∙min-1∙mmHg-1; p=0.41). The V̇E-PCO2 relationship is unaltered across a range of mild to extreme PO2. Brief exposure to normobaric hyperoxia may not independently stimulate breathing nor does it alter central chemoreflex sensitivity.

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Silva, Gisele S., and Aneesh B. Singhal. "Abstract W P42: Ischemic Lesions Grow, but NIHSS Scores Improve Over 48 Hours After Stroke: Implications for Clinical Trials." Stroke 45, suppl_1 (2014). http://dx.doi.org/10.1161/str.45.suppl_1.wp42.

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Background: DWI lesion growth is often used as a surrogate outcome measure in early-phase stroke clinical trials. Several studies have shown that admission DWI volumes and 3-mth clinical outcomes are strongly correlated, and that DWI volumes and NIHSS scores correlate at various times after stroke. However, there are few quantitative data comparing the dynamic changes of NIHSS scores to DWI lesion growth in acute ischemic stroke. Methods: We analyzed data from a phase II clinical trial of normobaric oxygen therapy (NBO) in acute ischemic stroke. Patients ineligible for tPA with imaging-confirmed ischemic stroke <9h and NIHSS>4 were randomized to NBO or Medical Air, delivered for 8h. There was no upper limit for age, NIHSS or stroke volume. NIHSS and DWI scans were obtained at 0 h, 4h (during therapy), 24h, and 48h. In this trial NBO had no significant effect on NIHSS change or DWI growth, hence data from NBO and Air groups were combined for this analysis. Results: Serial DWI and NIHSS were obtained in 60 subjects (mean age 72 yrs, 53% male). Mean DWI lesion volumes increased over time (baseline, 44 cc; 24 hrs, 68 cc and 48 hrs, 76 cc, p=0.1 ) but median NIHSS scores decreased over time (baseline, 12; 24 hrs, 10; 48 hrs, 9; p=0.1 ). There was no significant correlation between 0-24 hour change in NIHSS scores and 0-24 hour % DWI growth (r square=0.01, p=0.38), or absolute DWI growth (r square=0.033, p=0.21). There was no significant correlation between 0-48 hour change in NIHSS scores and 0-48 hour % DWI growth (r square 0.005, p=0.63), and only a mild correlation with absolute DWI growth (r square=0.11, p= 0.03). Stroke etiology affected these correlations: there was a significant correlation between NIHSS change and DWI growth at 48 hrs for cardio-embolic strokes, but not for large-artery strokes. Linear regression analysis adjusting for age, gender, mismatch and arterial recanalization status, showed that change in NIHSS was not associated with DWI growth neither at 24 ( p=0.41) nor at 48 hours (p=0.16). Conclusion: While the dynamic relationship between clinical deficits and lesion growth differs according to stroke mechanism, on average, infarcts grow but neuro deficits improve in the first few days after ischemic stroke. The mechanisms underlying this paradox require further study.

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