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Purpose Data on the benefit or or harmful effects of oxygen level on ischemic reperfusion injuries in cardiac surgery are insufficient. We hypothesized that hyperoxia during cardiopulmonary bypass decreases the incidence of postoperative atrial fibrillation (POAF) and ventricular fibrillation, and therefore decreases cardiovascular morbidity (CARDIOX study). Methods An open-label, randomized clinical trial including adults undergoing elective cardiac surgery, i.e. cardiopulmonary bypass (CPB) randomized 1:1 to an intervention group or standard group at two French University Hospitals from June 2016 to October 2018. The intervention consisted in delivering of an inspired fraction of oxygen of one to one during CPB. The standard care consisted in delivering oxygen to achieve a partial arterial blood pressure less than 150 mmHg. The primary endpoint was the occurrence of POAF and/or ventricular tachycardia/ventricular fibrillation (VT/VF) within the 15 days following cardiac surgery. The secondary endpoint was the occurrence of major adverse cardiovascular events (MACCE: in-hospital mortality, stroke, cardiac arrest, acute kidney injury, and mesenteric ischemia). Results 330 patients were randomly assigned to either the intervention group ( n  = 161) or the standard group ( n  = 163). Mean PaO 2 was 447 ± 98 mmHg and 161 ± 60 mmHg during CPB, for the intervention and standard group ( p  < 0.0001) respectively. The incidence of POAF or VT/VF were similar in the intervention group and the standard group (30% [49 of 161 patients] and 30% [49 of 163 patients], absolute risk reduction 0.4%; 95% CI, − 9.6–10.4; p  = 0.94). MACCE was similar between groups with, an occurrence of 24% and 21% for the intervention group and the standard groups (absolute risk reduction 3.4%; 95% CI, − 5.7–12.5; p  = 0.47) respectively. After adjustment, the primary and secondary endpoints remained similar for both groups. Conclusion Hyperoxia did not decrease POAF and cardiovascular morbidity following cardiac surgery with CPB. Clinicaltrial.gov identifier NCT02819739.

We developed a device (FreeO2) that automatically adjusts the oxygen flow rates based on patients' needs, in order to limit hyperoxia and hypoxemia and to automatically wean them from oxygen. The aim of this study was to evaluate the feasibility of using FreeO2 in patients hospitalized in the respiratory ward for an acute exacerbation of COPD. We conducted a randomized controlled trial comparing FreeO2 vs manual oxygen titration in the respiratory ward of a university hospital. We measured the perception of appropriateness of oxygen titration and monitoring in both groups by nurses and attending physicians using a Likert scale. We evaluated the time in the target range of oxygen saturation (SpO2) as defined for each patient by the attending physician, the time with severe desaturation (SpO2 <85%), and the time with hyperoxia (SpO2 >5% above the target). We also recorded length of stay, intensive care unit admissions, and readmission rate. Fifty patients were randomized (25 patients in both groups; mean age: 72±8 years; mean forced expiratory volume in 1 second: 1.00±0.49 L; and mean initial O2 flow 2.0±1.0 L/min). Nurses and attending physicians felt that oxygen titration and monitoring were equally appropriate with both O2 administration systems. The percentage of time within the SpO2 target was significantly higher with FreeO2, and the time with severe desaturation and hyperoxia was significantly reduced with FreeO2. Time from study inclusion to hospital discharge was 5.8±4.4 days with FreeO2 and 8.4±6.0 days with usual oxygen administration (P=0.051). FreeO2 was deemed as an appropriate oxygen administration system by nurses and physicians of a respiratory unit. This system maintained SpO2 at the target level better than did manual titration and reduced periods of desaturation and hyperoxia. Our results also suggest that FreeO2 has the potential to reduce the hospital length of stay.

Hypoxia and hyperoxia can affect the acute psycho-physiological response to exercise. Recording various perceptual responses to exercise is of particular importance for investigating behavioral changes to physical activity, given that the perception of exercise-induced pain, discomfort or unpleasure, and a low level of exercise enjoyment are commonly associated with a low adherence to physical activity. Therefore, this study aimed to compare the acute perceptual and physiological responses to aerobic exercise under intermittent hypoxia-hyperoxia (IHHT), hypoxia-normoxia (IHT), and sustained normoxia (NOR) in young, recreational active, healthy males. Using a randomized, single-blinded, crossover design, 15 males (age: 24.5 ± 4.2 yrs) performed 40 min of submaximal constant-load cycling (at 60% peak oxygen uptake, 80 rpm) under IHHT (5 × 4 min hypoxia and hyperoxia), IHT (5 × 4 min hypoxia and normoxia), and NOR. Inspiratory fraction of oxygen during hypoxia and hyperoxia was set to 14% and 30%, respectively. Heart rate (HR), total hemoglobin (tHb) and muscle oxygen saturation (S O ) of the right vastus lateralis muscle were continuously recorded during cycling. Participants' peripheral oxygen saturation (S O ) and perceptual responses ( ., perceived motor fatigue, effort perception, perceived physical strain, affective valence, arousal, motivation to exercise, and conflict to continue exercise) were surveyed prior, during (every 4 min), and after cycling. Prior to and after exercise, peripheral blood lactate concentration (BLC) was determined. Exercise enjoyment was ascertained after cycling. For statistical analysis, repeated measures analyses of variance were conducted. No differences in the acute perceptual responses were found between conditions ( ≥ 0.059, ≤ 0.18), while the physiological responses differed. Accordingly, S O was higher during the hyperoxic periods during the IHHT compared to the normoxic periods during the IHT ( < 0.001, = 0.91). Moreover, HR ( = 0.005, = 0.33) and BLC ( = 0.033, = 0.28) were higher during IHT compared to NOR. No differences between conditions were found for changes in tHb ( = 0.684, = 0.03) and S O ( = 0.093, = 0.16). IHT was associated with a higher physiological response and metabolic stress, while IHHT did not lead to an increase in HR and BLC compared to NOR. In addition, compared to IHT, IHHT seems to improve reoxygenation indicated by a higher S O during the hyperoxic periods. However, there were no differences in perceptual responses and ratings of exercise enjoyment between conditions. These results suggest that replacing normoxic by hyperoxic reoxygenation-periods during submaximal constant-load cycling under intermittent hypoxia reduced the exercise-related physiological stress but had no effect on perceptual responses and perceived exercise enjoyment in young recreational active healthy males.

Endothelin‐1 (ET‐1) and its receptors are linked to increases in sensitivity of the chemoreceptors to hypoxic stress and the development of hypertension in preclinical models. We hypothesized ET receptor antagonism would lower resting blood pressure (BP) as well as the acute BP response to chemoreflex stress. Twenty‐four men (31 ± 5 years, 26 ± 3 kg/m2) completed two study visits (control, bosentan). On each visit, BP was assessed under three conditions: (1) normoxia (FiO2 0.21), (2) chemoreflex excitation via hypoxia (FiO2 0.05–0.21), (3) chemoreflex inhibition via hyperoxia (FiO2 1.00). Bosentan increased plasma ET‐1 (0.94 ± 0.90 to 1.27 ± 0.62 pg/mL, p = 0.004), supporting receptor blockade. Resting diastolic (73 ± 5 to 69 ± 7 mmHg, p = 0.007) and mean (93 ± 7 to 88 ± 7 mmHg, p = 0.005) BP were reduced following bosentan compared to control with no change in systolic BP (p = 0.507). The mean BP response to both acute hypoxia (−0.48 ± 0.38 to −0.25 ± 0.31 mmHg/%, p = 0.004) and hyperoxia (area under the curve −93 ± 108 to −27 ± 66 AU, p = 0.018) were attenuated following bosentan. Acute ET receptor inhibition attenuates the rise in BP during chemoreflex excitation as well as the fall in BP during chemoreflex inhibition in healthy young men. These data support a role for ET‐1 in control of resting BP, possibly through a chemoreceptor‐mediated mechanism.

Background Anesthesiologists administer excess supplemental oxygen (hyper-oxygenation) to patients during surgery to avoid hypoxia. Hyper-oxygenation, however, may increase the generation of reactive oxygen species and cause oxidative damage. In cardiac surgery, increased oxidative damage has been associated with postoperative kidney and brain injury. We hypothesize that maintenance of normoxia during cardiac surgery (physiologic oxygenation) decreases kidney injury and oxidative damage compared to hyper-oxygenation. Methods/design The Risk of Oxygen during Cardiac Surgery (ROCS) trial will randomly assign 200 cardiac surgery patients to receive physiologic oxygenation, defined as the lowest fraction of inspired oxygen (FIO 2 ) necessary to maintain an arterial hemoglobin saturation of 95 to 97%, or hyper-oxygenation (FIO 2  = 1.0) during surgery. The primary clinical endpoint is serum creatinine change from baseline to postoperative day 2, and the primary mechanism endpoint is change in plasma concentrations of F 2 -isoprostanes and isofurans. Secondary endpoints include superoxide production, clinical delirium, myocardial injury, and length of stay. An endothelial function substudy will examine the effects of oxygen treatment and oxidative stress on endothelial function, measured using flow mediated dilation, peripheral arterial tonometry, and wire tension myography of epicardial fat arterioles. Discussion The ROCS trial will test the hypothesis that intraoperative physiologic oxygenation decreases oxidative damage and organ injury compared to hyper-oxygenation in patients undergoing cardiac surgery. Trial registration ClinicalTrials.gov, ID: NCT02361944 . Registered on the 30th of January 2015.

Hyperoxia causes hemodynamic alterations. We hypothesized that cardiovascular and autonomic control changes last beyond the end of hyperoxic period into normoxia. Ten healthy volunteers were randomized to breathe either medical air or 100% oxygen for 45 min in a double-blind study design. Measurements were performed before (baseline) and during gas exposure, and then 10, 30, 60, and 90 min after gas exposure. Hemodynamic changes were studied by Doppler echocardiography. Changes in cardiac and vasomotor autonomic control were evaluated through changes in spectral power of heart rate variability and blood pressure variability. Cardiac baroreflex sensitivity was assessed by the sequence method. Hyperoxia significantly decreased heart rate and increased the high frequency power of heart rate variability, suggesting a chemoreflex increase in vagal activity since the slope of cardiac baroreflex was significantly decreased during hyperoxia. Hyperoxia increased significantly the systemic vascular resistances and decreased the low frequency power of blood pressure variability, suggesting that hyperoxic vasoconstriction was not supported by an increase in vascular sympathetic stimulation. These changes lasted for 10 min after hyperoxia ( p  < 0.05). After the end of hyperoxic exposure, the shift of the power spectral distribution of heart rate variability toward a pattern of increased cardiac sympathetic activity lasted for 30 min ( p  < 0.05), reflecting a resuming of baseline autonomic balance. Cardiac output and stroke volume were significantly decreased during hyperoxia and returned to baseline values (10 min) later than heart rate. In conclusion, hyperoxia effects continue during return to normoxic breathing, but cardiac and vascular parameters followed different time courses of recovery.

Supratentorial pneumocephalus after posterior fossa surgery in the semisitting position may lead to decreased alertness and other symptoms. We here aimed to prove the efficacy of normobaric hyperoxia on the absorption of postoperative pneumocephalus according to a standardized treatment protocol. We enrolled 44 patients with postoperative supratentorial pneumocephalus (> 30 ml) after posterior fossa surgery in a semisitting position. After randomisation procedure, patients received either normobaric hyperoxia at FiO2 100% over an endotracheal tube for 3 hours (treatment arm) or room air (control arm). Routine cranial CT scans were performed immediately (CT1) and 24 hours (CT2) after completion of surgery and were rated without knowledge of the therapy arm. Two co-primary endpoints were assessed: (i) mean change of pneumocephalus volume, and (ii) air resorption rate in 24 hours. Secondary endpoints were subjective alertness (Stanford Sleepiness Scale) postoperatively and attention (Stroop test), which were evaluated preoperatively and 24 hours after surgery. The mean change in pneumocephalus volume was higher in patients in the treatment arm as compared to patients in the control arm (p = 0.001). The air resorption rate was higher in patients in the treatment arm as compared to patients in the control arm (p = 0.0015). Differences were more pronounced in patients aged 52 years and older. No difference between patients in treatment arm and control arm was observed for the Stroop test. The distribution of scores in the Stanford Sleepiness Scale differed in the treatment arm as compared to the control arm, and there was a difference in mean values (p = 0.015). Administration of normobaric hyperoxia at FiO2 100% via an endotracheal tube for 3 hours is safe and efficacious in the treatment of pneumocephalus after posterior fossa surgery in the semisitting position. Largest benefit was found in elderly patients and particularly in older men. German Clinical Trials Register DRKS00006273.

This investigation explored the influence of supplemental oxygen administered during the recovery periods of an interval-based running session on the post-exercise markers of reactive oxygen species (ROS) and inflammation. Ten well-trained male endurance athletes completed two sessions of 10 × 3 min running intervals at 85 % of the maximal oxygen consumption velocity ( vV O 2peak ) on a motorised treadmill. A 90-s recovery period was given between each interval, during which time the participants were administered either a hyperoxic (HYP) (Fraction of Inspired Oxygen (F I O 2 ) 99.5 %) or normoxic (NORM) (F I O 2 21 %) gas, in a randomized, single-blind fashion. Pulse oximetry (S p O 2 ), heart rate (HR), blood lactate (BLa), perceived exertion (RPE), and perceived recovery (TQRper) were recorded during each trial. Venous blood samples were taken pre-exercise, post-exercise and 1 h post-exercise to measure Interleukin-6 (IL-6) and Isoprostanes (F 2 -IsoP). The S p O 2 was significantly lower than baseline following all interval repetitions in both experimental trials ( p  < 0.05). The S p O 2 recovery time was significantly quicker in the HYP when compared to the NORM ( p  < 0.05), with a trend for improved perceptual recovery. The IL-6 and F 2 -IsoP were significantly elevated immediately post-exercise, but had significantly decreased by 1 h post-exercise in both trials ( p  < 0.05). There were no differences in IL-6 or F 2 -IsoP levels between trials. Supplemental oxygen provided during the recovery periods of interval based exercise improves the recovery time of S P O 2 but has no effect on post-exercise ROS or inflammatory responses.

Purpose We have argued that breathing 40 % O 2 attenuates exercise hyperaemia by decreasing production of O 2 -dependent vasodilators. However, breathing 100 % O 2 attenuated endothelium-dependent vasodilatation evoked by acetylcholine and this effect was prevented by vitamin C, implicating reactive oxygen species (ROS). We have therefore used vitamin C to test the hypothesis that 40 % O 2 modulates exercise hyperaemia and reactive hyperaemia independently of ROS. Method In a cross-over study on 10 male subjects (21.1 ± 0.84 years), we measured forearm blood flow (venous occlusion plethysmography) and calculated forearm vascular conductance (FVC) at rest and following static handgrip at 60 % maximum voluntary contraction for 2 min and following arterial occlusion for 2 min, after placebo or oral vitamin C (2000 mg), and when breathing air or 40 % O 2 . Result During air breathing, vitamin C augmented the peak increase in FVC following static contraction, or release of arterial occlusion, by ~50 or 60 %, respectively ( P  < 0.05). Breathing 40 % O 2 in the presence of placebo attenuated post-contraction hyperaemia by ~25 % ( P  < 0.05), but had no effect on reactive hyperaemia. By contrast, in the presence of vitamin C, 40 % O 2 attenuated the peak increase in FVC following static contraction, or release of arterial occlusion by ~25 and 50 %, respectively ( P  < 0.05). Conclusion These results indicate that in young men, exercise hyperaemia following strenuous muscle contraction and reactive hyperaemia are blunted by ROS. However, they are also consistent with the view that modest hyperoxia induced by breathing 40 % O 2 acts independently of ROS to attenuate not only post-contraction hyperaemia, but also reactive hyperaemia, by decreasing release of O 2 -dependent vasodilators.

During late lung development, alveolar and microvascular development is finalized to enable sufficient gas exchange. Impaired late lung development manifests as bronchopulmonary dysplasia (BPD) in preterm infants. Single-cell RNA sequencing (scRNA-seq) allows for assessment of complex cellular dynamics during biological processes, such as development. Here, we use MULTI-seq to generate scRNA-seq profiles of over 66,000 cells from 36 mice during normal or impaired lung development secondary to hyperoxia with validation of some of the findings in lungs from BPD patients. We observe dynamic populations of cells, including several rare cell types and putative progenitors. Hyperoxia exposure, which mimics the BPD phenotype, alters the composition of all cellular compartments, particularly alveolar epithelium, stromal fibroblasts, capillary endothelium and macrophage populations. Pathway analysis and predicted dynamic cellular crosstalk suggest inflammatory signaling as the main driver of hyperoxia-induced changes. Our data provides a single-cell view of cellular changes associated with late lung development in health and disease. It is unclear how changes in gene expression are induced by changes in oxygen levels during late lung development. Here, the authors provide data from MULTI-seq scRNAseq in mice showing exposure to higher oxygen levels affects cell fates, especially for alveolarisation, and define gene/cell signatures of impaired lung development under hyperoxia.