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BACKGROUND: When treating acute respiratory failure, both hypoxemia and hyperoxemia should be avoided. ... should be monitored closely and O2 flows adjusted accordingly. Achieving this goal might be easier with automated O2 titration compared with manual titration of fixed-flow O2. We evaluated the feasibility of using an automated O2 titration device in subjects treated for acute hypoxemic respiratory failure in a tertiary care hospital. METHODS: Health-care workers received education and training about oxygen therapy, and were familiarized with an automated O2 titration device (FreeO2,). A coordinator was available from 8:00 AM to 5:00 PM during weekdays to provide technical assistance. The ability of the device to maintain ... within the prescribed therapeutic window was recorded. Basic clinical information was recorded. RESULTS: Subjects were enrolled from November 2020 to August 2022. We trained 508 health-care workers on the use of automated O2 titration, which was finally used on 872 occasions in 763 subjects, distributed on the respiratory, COVID-19, and thoracic surgery wards, and in the emergency department. Clinical information could be retrieved for 609 subjects (80%) who were on the system for a median (interquartile range) of 3 (2-6) d, which represented 2,567 subject-days of clinical experience with the device. In the 82 subjects (14%) for whom this information was available, the system maintained ... within the prescribed targets 89% of the time. Ninety-six subjects experienced clinical deterioration as defined by the need to be transferred to the ICU and/or requirement of high flow nasal oxygen but none of these events were judged to be related to the O2 device. CONCLUSIONS: Automated O2 titration could be successfully implemented in hospitalized subjects with hypoxemic respiratory failure from various causes. This experience should foster further improvement of the device and recommendations for an optimized utilization. [ABSTRACT FROM AUTHOR]

Oxygen therapy provides an important treatment for preterm and low-birth-weight neonates, however, it has been shown that prolonged exposure to high levels of oxygen (hyperoxia) is one of the factors contributing to the development of bronchopulmonary dysplasia (BPD) by inducing lung injury and airway hyperreactivity. There is no effective therapy against the adverse effects of hyperoxia. Therefore, this study was undertaken to test the hypothesis that natural phytoalexin resveratrol will overcome hyperoxia-induced airway hyperreactivity, oxidative stress, and lung inflammation. Newborn rats were exposed to hyperoxia (fraction of inspired oxygen - FiO2>95 % O2) or ambient air (AA) for seven days. Resveratrol was supplemented either in vivo (30 mg·kg-1·day-1) by intraperitoneal administration or in vitro to the tracheal preparations in an organ bath (100 µM). Contractile and relaxant responses were studied in tracheal smooth muscle (TSM) using the in vitro organ bath system. To explain the involvement of nitric oxide in the mechanisms of the protective effect of resveratrol against hyperoxia, a nitric oxide synthase inhibitor - Nω-nitro-L-arginine methyl ester (L-NAME), was administered in some sets of experiments. The superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and the tumor necrosis factor-alpha (TNF-α) and interleukin-1γ (IL-1γ) levels in the lungs were determined. Resveratrol significantly reduced contraction and restored the impaired relaxation of hyperoxia-exposed TSM (p<0.001). L-NAME reduced the inhibitory effect of resveratrol on TSM contractility, as well as its promotion relaxant effect (p<0.01). Resveratrol preserved the SOD and GPx activities and decreased the expression of TNF-α and IL-1γ in hyperoxic animals. The findings of this study demonstrate the protective effect of resveratrol against hyperoxia-induced airway hyperreactivity and lung damage and suggest that resveratrol might serve as a therapy to prevent the adverse effects of neonatal hyperoxia. [ABSTRACT FROM AUTHOR]

OBJECTIVE: It is known that providing recanalization alone in large vessel occlusions is not sufficient to provide a good 90-day clinical outcome. It is advocated that neuroprotection should be increased before endovascular treatment and that the penumbra should be protected from reperfusion damage after recanalization. However, the effects of blood gas parameters before and after mechanical thrombectomy on clinical outcomes are not clear. The objective of this study is to assess the effectiveness of serial blood gas measures in accurately predicting futile recanalization at an early stage. PATIENTS AND METHODS: This study is a multicenter inquiry that collected data in a prospective manner and analyzed it retrospectively. Patients with a 2b-3 thrombolysis in cerebral infarction (TICI) score after mechanical thrombectomy for recanalization were consecutively analyzed from July 2022 to March 2023. Arterial blood gas parameters, including pH, oxygen saturation (SaO2), partial carbon dioxide pressure (PaCO2), partial oxygen pressure (PaO2), lactate, and bicarbonate (HCO3), were measured at four time points: before mechanical thrombectomy treatment (preoperative), immediately after recanalization (postoperative 1st), during the 3rd hour (postoperative 3rd), and at the 5th hour (postoperative 5th). The patients were categorized into groups based on their modified Rankin Scale (mRS) scores. RESULTS: The study included 136 patients with an average age of 69.71±11.22. The postoperative 1st-hour SaO2 values were lower in the mRS 3-6 group (p=0.038). The postoperative pH and lactate mean were greater in the mRS 3-6 group than in the 0-2 group (p=0.038 and 0.018, respectively). In logistic regression, a unit rise in lactate increased poor functional outcomes 1,632 times (p=0.024). Early neurological recovery was associated with decreased postoperative 3rd-hour lactate (p=0.014). The mean postoperative PaO2 (average of 1, 2, 3 PaO2) was higher in those with symptomatic cerebral bleeding (p=0.044). CONCLUSIONS: Monitoring lactate and pH levels in AIS patients who have had mechanical recanalization can be utilized to predict mortality and morbidity, especially in the first five hours after the procedure. [ABSTRACT FROM AUTHOR]

In recent years, a lot of controversies have emerged regarding conservative versus liberal oxygen therapy in critically ill patients. While neurologically injured patients might have higher oxygen demand due to high cerebral metabolism, recent studies have clearly shown that hyperoxia may not be beneficial in improving the neurological outcome in traumatic brain injury, subarachnoid hemorrhage, and acute ischemic stroke. Rather, hyperoxia might worsen neurological outcome in such conditions by various mechanisms like direct cerebral vasoconstriction or by increased excitotoxicity, which in turn leads to lipid peroxidation and generation of harmful reactive oxygen species. This article brings into insight the current evidence on the effect of hyperoxia on these three acute neurological insults. [ABSTRACT FROM AUTHOR]

Hyperbaric oxygen (HBO) therapy involves intermittent inhalation by the patient of 100% oxygen under a pressure greater than 1 atmosphere. Both therapeutic and toxic effects can result from two features of this form of treatment; mechanical effects arising from exposure to increased ambient pressure and the physiological effects of hyperoxia. Substantial evidence supports the use of HBO therapy in certain carefully defined settings, though many patients who might benefit go untreated because of their physicians' unfamiliarity with recent research and overall uncertainty about the legitimacy of HBO as a therapy. The author discusses the mechanism of action of HBO therapy and the commonly accepted clinical indications. [ABSTRACT FROM AUTHOR]

Introduction: Previous studies have highlighted hyperoxia-induced microcirculation modifications, but few have focused on hyperbaric oxygen (HBO) effects. Our primary objective was to explore hyperbaric hyperoxia effects on the microcirculation of healthy volunteers and investigate whether these modifications are adaptative or not. Methods: This single centre, open-label study included 15 healthy volunteers. Measurements were performed under five conditions: T0) baseline value (normobaric normoxia); T1) hyperbaric normoxia; T2) hyperbaric hyperoxia; T3) normobaric hyperoxia; T4) return to normobaric normoxia. Microcirculatory data were gathered via laser Doppler, near-infrared spectroscopy and transcutaneous oximetry (PtcO2). Vascular-occlusion tests were performed at each step. We used transthoracic echocardiography and standard monitoring for haemodynamic investigation. Results: Maximal alterations were observed under hyperbaric hyperoxia which led, in comparison with baseline, to arterial hypertension (mean arterial pressure 105 (SD 12) mmHg vs 95 (11), P < 0.001) and bradycardia (55 (7) beats·min-1 vs 66 (8), P < 0.001) while cardiac output remained unchanged. Hyperbaric hyperoxia also led to microcirculatory vasoconstriction (rest flow 63 (74) vs 143 (73) perfusion units, P < 0.05) in response to increased PtcO2 (104.0 (45.9) kPa vs 6.3 (2.4), P < 0.0001); and a decrease in laser Doppler parameters indicating vascular reserve (peak flow 125 (89) vs 233 (79) perfusion units, P < 0.05). Microvascular reactivity was preserved in every condition. Conclusions: Hyperoxia significantly modifies healthy volunteer microcirculation especially during HBO exposure. The rise in PtcO2 promotes an adaptative vasoconstrictive response to protect cellular integrity. Microvascular reactivity remains unaltered and vascular reserve is mobilised in proportion to the extent of the ischaemic stimulus. [ABSTRACT FROM AUTHOR]

Introduction: This study measured pulmonary function in divers after a single helium-oxygen (heliox) dive to 80, 100, or 120 metres of sea water (msw). Methods: A total of 26 divers participated, of whom 15, five, and six performed a 80, 100, or 120 msw dive, respectively. While immersed, the divers breathed heliox and air, then oxygen during surface decompression in a hyperbaric chamber. Pulmonary function was measured twice before diving, 30 min after diving, and 24 h after diving. Results: At 30 min after the 80 msw dive the forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ratio and the maximum expiratory flow at 25% of vital capacity (MEF25) values decreased (89.2% to 87.1% and 2.57 L·s-1 to 2.35 L·s-1, P = 0.04, P = 0.048 respectively) but FEV1/FVC returned to the baseline values by 24 h post-dive. Other pulmonary indicators exhibited downward trends at 30 min after the dive, but statistical significance was lacking. Interestingly, though several parameters decreased after the 100 msw dive, statistical significance was not reached. After the 120 msw dive, the FEV1/FVC and MEF75 decreased (90.4% to 85.6% and 8.05 L·s-1 to 7.46 L·s-1, P = 0.01, P = 0.007). The relatively small numbers of subjects who dived to 100 and 120 msw depths may explain the inconsistent results. The subjects diving to 100 and 120 msw were more trained / skilled, but this would not explain the inconsistencies in results between these depths. Conclusions: We conclude that single deep heliox dives cause a temporary decrease in FEV1/FEV and MEF25 or MEF75, but these changes can recover at 24 h after the dive. [ABSTRACT FROM AUTHOR]

To describe the current nationwide perspectives and practice regarding intraoperative oxygen titration in cardiac surgery. Prospective, observational survey. Hospitals across the United States. Cardiovascular anesthesiologists and perfusionists. Expert- and consensus-derived electronic surveys were sent to perfusionists and cardiac anesthesiologists to evaluate the current intraoperative practices around oxygen administration. Providers were asked about individual intraoperative oxygen titration practices used at different stages of cardiac surgical procedures. Anonymous responses were collected in the Research Electronic Data Capture (REDCap). A total of 3,335 providers were invited to participate, of whom 554 (317 anesthesiologists and 237 perfusionists) were included in the final analysis (17% response rate). During cardiopulmonary bypass (CPB), perfusionists reported a median (interquartile range [IQR]) target range from 150 (110-220)-to-325 mmHg (250-400), while anesthesiologists reported a significantly lower target range from 90 (70-150)-to-250 mmHg (158-400) (p values <0.0001 and 0.02, respectively). This difference was most pronounced at lower partial pressure of arterial oxygen (PaO 2) ranges. The median PaO 2 considered "too low" by perfusionists was 100 mmHg (IQR 80-125), whereas it was 60 mmHg (IQR 60-75) for anesthesiologists, who reported for both off and on bypass. The median PaO 2 considered "too high" was 375 mmHg (IQR 300-400) for perfusionists and 300 mmHg (IQR 200-400) for anesthesiologists. Anesthesiologists, therefore, reported more comfort with significantly lower PaO 2 values (p < 0.0001), and considered a higher PaO 2 value less desirable compared with perfusionists (p < 0.0001). This survey demonstrated there was wide variation in oxygen administration practices between perfusionists and anesthesiologists. Hyperoxygenation was more common while on CPB. [ABSTRACT FROM AUTHOR]

To describe the current nationwide perspectives and practice regarding intraoperative oxygen titration in cardiac surgery. Prospective, observational survey. Hospitals across the United States. Cardiovascular anesthesiologists and perfusionists. Expert- and consensus-derived electronic surveys were sent to perfusionists and cardiac anesthesiologists to evaluate the current intraoperative practices around oxygen administration. Providers were asked about individual intraoperative oxygen titration practices used at different stages of cardiac surgical procedures. Anonymous responses were collected in the Research Electronic Data Capture (REDCap). A total of 3,335 providers were invited to participate, of whom 554 (317 anesthesiologists and 237 perfusionists) were included in the final analysis (17% response rate). During cardiopulmonary bypass (CPB), perfusionists reported a median (interquartile range [IQR]) target range from 150 (110-220)-to-325 mmHg (250-400), while anesthesiologists reported a significantly lower target range from 90 (70-150)-to-250 mmHg (158-400) (p values <0.0001 and 0.02, respectively). This difference was most pronounced at lower partial pressure of arterial oxygen (PaO 2) ranges. The median PaO 2 considered "too low" by perfusionists was 100 mmHg (IQR 80-125), whereas it was 60 mmHg (IQR 60-75) for anesthesiologists, who reported for both off and on bypass. The median PaO 2 considered "too high" was 375 mmHg (IQR 300-400) for perfusionists and 300 mmHg (IQR 200-400) for anesthesiologists. Anesthesiologists, therefore, reported more comfort with significantly lower PaO 2 values (p < 0.0001), and considered a higher PaO 2 value less desirable compared with perfusionists (p < 0.0001). This survey demonstrated there was wide variation in oxygen administration practices between perfusionists and anesthesiologists. Hyperoxygenation was more common while on CPB. [ABSTRACT FROM AUTHOR]

Current guidelines emphasize the use of 100% oxygen during cardiopulmonary resuscitation after cardiac arrest. When patients are ventilated for variable periods after return of spontaneous circulation (ROSC), hyperoxia causes increased morbidity and mortality by overproduction of reactive oxygen species. Various patient, volunteer, and animal studies have shown the harmful effects of hyperoxia. This mini-review article aims to expand the potential clinical spectrum of hyperoxia on individual organ systems leading to organ dysfunction. A framework to achieve and maintain normoxia after ROSC is proposed. Despite the harmful considerations of hyperoxia in critically ill patients, additional safety studies including dose-effect, level and onset of the reactive oxygen species effect, and safe hyperoxia applicability period after ROSC, need to be performed in various animal and human models to further elucidate the role of oxygen therapy after cardiac arrest. [ABSTRACT FROM AUTHOR]

• Postoperative hyperoxia was common in patients after cardiopulmonary bypass (CPB). • This study assessed the association between partial pressure of oxygen trajectory and acute kidney injury (AKI) in CPB patients. • Persistent hyperoxia was associated with increased AKI incidence. To investigate the impact of the dynamic oxygenation status on the incidence of acute kidney injury (AKI) in patients undergoing cardiopulmonary bypass. This retrospective study was performed using data extracted from the Medical Information Mart for Intensive Care III database. A group-based trajectory approach was used to identify partial pressure of oxygen (PaO 2) trajectories using dynamic change in PaO 2 within 48 hours after intensive care unit admission. In total, 5,824 patients were included. Four PaO 2 trajectories were identified: Trajectory 1 (Traj-1), hyperoxia and rapid decrease; Trajectory 2 (Traj-2), hyperoxia and rapid decrease similar to that of Traj-1; Trajectory 3 (Traj-3), normoxemia and rapid increase in PaO 2 ; and Trajectory 4 (Traj-4), hyperoxia and gradual decrease. Compared with the Traj-1 group, the Traj-3 group had a significantly lower initial Sequential Organ Failure Assessment score, similar vasopressor use rate, and a higher fraction of inspired oxygen. However, the risk of developing AKI was significantly higher in the Traj-3 [adjusted odds ratio (OR): 1.7, 95% confidence interval (CI): 1.1–2.7] and Traj-4 groups (OR: 1.9, 95% CI: 1.4–2.5) than in the Traj-1 group. Patients with persistent hyperoxia had a higher incidence of AKI than those with transient hyperoxia. Further studies are required to determine potential underlying mechanisms. [Display omitted] [ABSTRACT FROM AUTHOR]

• Arterial hyperoxia (admission PaO2 >150 mmHg) was present in 20% of CICU patients • A J-shaped association was observed between admission PaO2 and mortality • A higher admission PaO2 was incrementally associated with higher mortality • Patients with severe hyperoxia (admission PaO2 >300 mmHg) were at highest risk of mortality Arterial hyperoxia (hyperoxemia), defined as a high arterial partial pressure of oxygen (PaO2), has been associated with adverse outcomes in critically ill populations, but has not been examined in the cardiac intensive care unit (CICU). We evaluated the association between exposure to hyperoxia on admission with in-hospital mortality in a mixed CICU cohort. We included unique Mayo Clinic CICU patients admitted from 2007 to 2018 with admission PaO2 data (defined as the PaO2 value closest to CICU admission) and no hypoxia (PaO2 < 60mmHg). The admission PaO2 was evaluated as a continuous variable and categorized (60-100 mmHg, 101-150 mmHg, 151-200 mmHg, 201-300 mmHg, >300 mmHg). Logistic regression was used to evaluate predictors of in-hospital mortality before and after multivariable adjustment. We included 3,368 patients with a median age of 70.3 years; 70.3% received positive-pressure ventilation. The median PaO2 was 99 mmHg, with a distribution as follows: 60-100 mmHg, 51.9%; 101-150 mmHg, 28.6%; 151-200 mmHg, 10.6%; 201-300 mmHg, 6.4%; >300 mmHg, 2.5%. A J-shaped association between admission PaO2 and in-hospital mortality was observed, with a nadir around 100 mmHg. A higher PaO2 was associated with increased in-hospital mortality (adjusted OR 1.17 per 100 mmHg higher, 95% CI 1.01-1.34, p = 0.03). Patients with PaO2 >300 mmHg had higher in-hospital mortality versus PaO2 60-100 mmHg (adjusted OR 2.37, 95% CI 1.41-3.94, p < 0.001). Hyperoxia at the time of CICU admission is associated with higher in-hospital mortality, primarily in those with severely elevated PaO2 >300 mmHg. [ABSTRACT FROM AUTHOR]

Introduction: Measurement of skin temperature with infrared thermometry has been utilised for assessing metabolic activity and may be useful in identifying patients with ulcers suitable for hyperbaric oxygen treatment and monitoring their treatment progress. Since oxygen promotes vasoconstriction in the peripheral circulation, we hypothesised that oxygen administration may lower skin temperature and complicate the interpretation of temperatures obtained. This pilot study investigated the effect of oxygen administration on lower limb skin temperature in healthy subjects and diabetic patients. Methods: Volunteers were recruited from healthy staff members (n = 10) and from patients with diabetic foot ulcers (n = 10) at our facility. Foot skin surface temperatures were measured by infra-red thermometry while breathing three different concentrations of oxygen (21%, 50% and 100%). Results: Skin temperature changes were observed with increasing partial pressure of oxygen in both groups. The mean (SD) foot temperatures of diabetic patients and healthy controls at air-breathing baseline were 30.1°C (3.6) versus 29.0°C (3.7) respectively, at FiO2 0.5 were 30.1°C (3.6) versus 28.5°C (4.1) and at FiO2 1.0 were 28.3°C (3.2) versus 29.2°C (4.3). None of these differences between groups were statistically significant. Conclusions: Data from this small study may indicate a difference in thermal responses between healthy subjects and diabetic patients when inhaling oxygen; however, none of the results were statistically significant. Further investigations on a larger scale are warranted in order to draw firm conclusions. [ABSTRACT FROM AUTHOR]

Background: Individuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm.Methods: Sprague-Dawley pups were exposed to room air (controls) or 80% O2 at postnatal days 3 to 10 (oxygen-induced cardiomyopathy). We studied left ventricle mitochondrial changes in 4 weeks old males. In a cohort of young adults born preterm (n=55) and age-matched term (n=54), we compared circulating levels of humanin.Results: Compared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced Nrf2 gene expression. In the cohort, left ventricle ejection fraction and peak global longitudinal strain were similar between groups however humanin levels were lower in preterm and associated with left ventricle ejection fraction and peak global longitudinal strain.Conclusions: In conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609. [ABSTRACT FROM AUTHOR]

This study examined performance and physiological responses (power output, tissue saturation index) to repeat sprint cycling with oxygen supplementation (O2Supp [fraction of inspired oxygen 1.00]). Fourteen amateur male cyclists took part. Two visits to the laboratory entailed; 15min relative intensity warm-up, 10min of passive recovery, followed by 10x15s repeated sprints, during which air inspired had FiO2 1.00 oxygen or normal air. Outcome measures include, mean power (W) and change in Tissue Saturation Index (TSI%). Repeated measures ANOVA were used to examine difference between conditions in mean power output. Paired samples t-tests were used to examine differences between conditions in TSI (%) and rate of muscle reoxygenation and deoxygenation (%·s-1). Mean power output was 4% higher in the oxygen condition compared to normoxia (p < .01). There was a significant positive correlation between power output and reoxygenation rate during O2Supp (r = 0.65, p = .04). No correlation was seen between power output and reoxygenation rate during normoxia (r = -0.30, p = .40). A significantly increased deoxy rate was seen in the O2Supp condition compared to normoxia (p = .05). Oxygen supplementation appears to elicit the greatest performance improvements in mean power, potentially facilitated by an increasing muscle reoxygenation rate. This evidences the utility of oxygen as an ergogenic aid to in cycling performance. [ABSTRACT FROM AUTHOR]

Introduction: Hyperbaric oxygen (HBO) exposure for 10-15 min has been shown to reduce peripheral blood flow due to vasoconstriction. However, the relationship between decreased peripheral blood flow and the therapeutic effects of HBO treatment on peripheral circulatory disorders remain unknown. Longer exposures have been reported to have vasodilatory effects and increase peripheral blood flow. This study investigated the effect of HBO treatment on blood flow and transcutaneous oxygen pressure (TcPO2). Methods: Twenty healthy volunteers aged 20--65 years (nine males) participated in this study. All participants breathed oxygen for 60 min at 253.3 kPa. Peripheral blood flow using laser Doppler flowmetry and TcPO2 on the ear, hand, and foot were continuously measured from pre-HBO exposure to 10 min post-exposure. Results: Peripheral blood flow in each body part decreased by 7--23% at the beginning of the HBO exposure, followed by a slow increase. Post-exposure, peripheral blood flow increased 4--76% in each body part. TcPO2 increased by 840-1,513% during the exposure period, and remained elevated for at least 10 min after the exposure. Conclusions: The findings of the current study suggest vasoconstriction during HBO treatment is transient, and even when present does not inhibit the development of increased tissue oxygen partial pressure. These findings are relevant to studies investigating changes in peripheral blood flow during HBO treatment in patients with circulatory disorders. [ABSTRACT FROM AUTHOR]

Intravenous thrombolysis elevates the prognostic level of acute ischemic stroke (AIS) patients. Normobaric hyperoxia (NBO) delays the progression of the infarct core and promotes neurological recovery. However, it is uncertain whether NBO can further raise the prognostic level of AIS patients based on intravenous thrombolysis. To explore the efficacy and safety of NBO combined with intravenous thrombolysis on AIS patients. This observational study included anterior circulation stroke patients who received intravenous thrombolysis within 4.5 h after stroke onset. These patients were divided into two groups based on whether or not they received NBO therapy. The baseline data and the prognosis of the two groups were compared. The primary outcome was the proportion of functional independence (modified Rankin Scale 0–2) at 90 days post discharge. A total of 227 patients were included in this study. 125 patients received NBO therapy combined with intravenous thrombolysis, while 102 patients received intravenous thrombolysis only. Overall, the rate of recanalization was 83.3%. Consequently, 101 patients (80.8%) who received NBO combined with intravenous thrombolysis and 63 patients (61.8%) in the control group achieved functional independence (P = 0.002). Multivariable logistic regression analysis showed that NBO combined with intravenous thrombolysis over intravenous thrombolysis alone was associated with 90-day functional independence (OR: 2.318; 95% CI: 1.226–4.381; P = 0.01). This study verified the efficacy and safety of NBO combined with intravenous thrombolysis in AIS patients. Prospective study is needed to further substantiate these findings. [ABSTRACT FROM AUTHOR]

Optimal oxygen management during cardiac surgery has not been established, and studies on the effects of perioperative hyperoxia on postoperative acute kidney injury (AKI) are scarce. The association between intraoperative hyperoxia and AKI after cardiac surgery involving cardiopulmonary bypass was evaluated for the present study. Retrospective observational study. A tertiary teaching hospital. Adult patients who underwent cardiac surgery with cardiopulmonary bypass from November 2006–December 2018. None. The area above arterial oxygen partial pressure (PaO 2) threshold of 300 mmHg (AOT 300 , mmHg × h) was used as a metric of intraoperative hyperoxia and was associated with postoperative AKI, using the logistic regression analysis. Data also were fitted using the restricted cubic spline model. Sensitivity analyses were conducted using different PaO 2 thresholds (150, 200, 250, and 350 mmHg). A total of 2,926 patients were analyzed. Intraoperative AOT 300 independently was associated with the risk of AKI (odds ratio 1.0009; 95% confidence interval 1.0002-1.0015). A PaO 2 increment of 100 mmHg above PaO 2 300 mmHg for an hour was associated with an increased risk of AKI by 9.4% (1.0009100 ≈ 1.094). In the spline model, the log-odds of AKI increased as AOT 300 increased. In the sensitivity analyses, AOT 250 and AOT 350 also significantly were associated with the risk of AKI, whereas AOT 150 and AOT 200 were not. As the PaO 2 threshold increased from 150 to 350 mmHg, the odds ratio gradually increased. Intraoperative hyperoxia significantly was associated with the risk of AKI after cardiac surgery involving cardiopulmonary bypass. [ABSTRACT FROM AUTHOR]

The use of oxygen therapy (high doses of oxygen - hyperoxia) in the treatment of premature infants results in their survival. However, it also results in a high incidence of chronic lung disease known as bronchopulmonary dysplasia, a disease in which airway hyper-responsiveness and pulmonary hypertension are well known as consequences. In our previous studies, we have shown that hyperoxia causes airway hyper-reactivity, characterized by an increased constrictive and impaired airway smooth muscle relaxation due to a reduced release of relaxant molecules such as nitric oxide, measured under in vivo and in vitro conditions (extra- and intrapulmonary) airways. In addition, the relaxation pathway of the vasoactive intestinal peptide (VIP) and/or pituitary adenylate cyclase activating peptide (PACAP) is another part of this system that plays an important role in the airway caliber. Peptide, which activates VIP cyclase and pituitary adenylate cyclase, has prolonged airway smooth muscle activity. It has long been known that VIP inhibits airway smooth muscle cell proliferation in a mouse model of asthma, but there is no data about its role in the regulation of airway and tracheal smooth muscle contractility during hyperoxic exposure of preterm newborns. [ABSTRACT FROM AUTHOR]

Iron is essential for cell growth, differentiation, electron transfer, and oxygen transport. Hyperoxia may increase the turnover of bone matrix components with a net effect of accelerated bone growth. Although hyperoxia was claimed could increase osteoblast activity, but expression level in possible genes which play role in proliferation is still unclear. This research aims to prove the differences of expression level of transferrin receptor gene and iron regulated transporter and other genes of 7F2 under 24 h normoxia, 24 h hyperoxia, and 48 h hyperoxia and the effect of hyperoxia by using osteoblast cell culture 7F2. Reverse transcriptase, real time Polymerase Chain Reaction (PCR), and microarray is used to qualitatively detect gene expression. The computer softwares such as National Center for Biotechnology Information (NCBI) data base, Software Affymetrix, DNA Strider program, Genomatix – DiAlign program, Oligo 5.0 program (Software primer design) from Wojciech & Piotr Rychlik, and Genetyx-Mac version 8.0 have been used to analyze the PCR result. Under 24 h hyperoxia, there were 3,884 copies of transferrin receptor mRNA per 1,000,000 copies of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) mRNA. After 24 h hyperoxia, 8,325 copies of transferrin receptor mRNA per 1,000,000 GAPDH mRNA copies were found showing 2.1-fold up regulation. After 48 h hyperoxia, there was no significant increase at the level of expression of transferrin receptor mRNA, 8,079 mRNA copies per 1,000,000 copies of mRNA were found (2.0-fold up regulation compared with 24 h normoxia). It can be concluded that hyperoxia might have an effect on upregulating the expression of some osteoblast genes which might have an impact on osteoblast activity. [ABSTRACT FROM AUTHOR]

• Our research mainly focuses on the effects of bioactive peptides from human milk on respiratory system development in preterm infants. • We derived from human breast milk, and MDABP could improve alveolar simplification and pulmonary vascular retardation. • Human milk-derived peptide MDABP ameliorates hyperoxia lung damage via inhibiting the ferroptosis signaling pathway. Human breast milk, the best source of nutrition for newborns, can reduce the incidence of bronchopulmonary dysplasia (BPD). Bioactive peptides are important components of human breast milk. However, their function in BPD are unclear. We screened a novel peptide (named MDABP) in the breast milk of mothers of premature infants, which has beneficial effects in experimental BPD. This study aimed to investigate the role and mechanism of MDABP in vivo and vitro. Newborn Sprague-Dawley (SD) rats were exposed to normoxia (21 % O 2) or hyperoxia (85 % O 2) and injected with MDABP or PBS from postnatal days 1 to 7 (PN1-PN7). On PN7, the lungs were harvested for histological and biochemical analysis. The results revealed that MDABP improved alveolar simplification and pulmonary vascular retardation, promoted alveolar epithelial cell (AEC) proliferation and inhibited cell apoptosis. In vitro , MDABP, but not scrambled MDABP, promoted cell proliferation and reduced cell injury without obvious toxicities. RNA-sequencing in A549 cells showed a total of 214 genes were significantly differentially expressed between the MDABP + hyperoxia and hyperoxia groups, including 80 upregulated and 134 downregulated genes. KEGG pathway analysis showed that significant differentially expressed genes were related to the ferroptosis signaling pathway. Rescue experiments showed that MDABP reduced the hyperoxia- and ferroptosis-induced damage to AEC by decreasing the levels of Fe2+ and ROS and increasing the levels of GSH and GPX4. The p-value of the above experiment was less than 0.05, which was considered statistically significant. This study provides a new basis for developing treatments for BPD. [ABSTRACT FROM AUTHOR]

BACKGROUND: Liberal oxygenation during mechanical ventilation is harmful in critically ill patients and in certain subsets of patients, including those with stroke, acute myocardial infarction, and cardiac arrest. Surveillance through electronic medical records improves safety of mechanical ventilation in the ICU. To date, this practice has not been used for oxygen titration (...) in adults. We hypothesize that a surveillance system based on the electronic medical record to alert respiratory therapists to titrate ... is feasible, safe, and efficacious. METHODS: In this pilot study, mechanically ventilated subjects were randomized to respiratory therapistdriven ... titration after an electronic alert versus standard of care (ie, titration based on physician order). An automated surveillance system utilizing a hyperoxemia-detection algorithm generated an electronic alert to a respiratory therapist's pager. Hyperoxemia was defined as ... > 0.5 and ... > 95% for > 30 min. No other aspects of treatment were changed. We assessed feasibility, safety, and preliminary efficacy. Primary outcome was duration of hyperoxemia during mechanical ventilation. An unsafe outcome was identified as hypoxemia (... < 88%) within 1 h after titration per alert. Feasibility was assessed by a survey of respiratory therapists. RESULTS: Of 226 randomized subjects, 31 were excluded (eg, programming errors of the electronic alerts, no consent, physician discretion). We included 195 subjects, of whom 86 were in the intervention arm. Alert accuracy was 78%, and respiratory therapists responded to 64% of the alerts. During mechanical ventilation, exposure to hyperoxemia significantly decreased in the intervention group (median 13.5 h [interquartile range 6.2-29.4] vs 18.8 h [interquartile range 9.6-37.4]). No episodes of significant hypoxemia were registered. Most respiratory therapists agreed that the alert was helpful in reducing excessive oxygen exposure. CONCLUSIONS: Use of an electronic surveillance system to titrate ... was safe and feasible and showed preliminary efficacy in reducing hyperoxemia. Our study serves to justify larger randomized controlled trials for ... titration. [ABSTRACT FROM AUTHOR]

Background: Supplemental oxygen is often required to treat preterm infants with respiratory disorders. Experimental studies have demonstrated that hyperoxia results in the disruption of intestinal and neuronal plasticity and myelination of the brain. The association between the neonatal hyperoxia and changes of phenotypes in gut microbiota and in behaviors is not clear to date. Methods: We designed an animal experiment that C57BL/6 mice pups were reared in either room air (RA) or hyperoxia (85% O2) from postnatal days 1 to 7. From postnatal days 8 to 42, the mice were reared in RA. Intestinal microbiota was sampled from the lower gastrointestinal tract on postnatal days 7 and 42, and behavioral tests were performed and brain tissues were collected on postnatal day 42. Results: Neonatal hyperoxia decreased intestinal tight junction protein expression and altered intestinal bacterial composition and diversity on postnatal day 7. Among the concrete discriminative features, Proteobacteria and Epsilonbacteraeota were significantly elevated in hyperoxia-reared mice on postnatal days 7 and 42, respectively. Hyperoxia-reared mice exhibited significantly reduced sociability and interest in social novelty and impaired motor coordination compared with RA-reared mice on postnatal day 42. Hyperoxia-reared mice also exhibited significantly reduced myelination and a significantly higher number of apoptotic cells in the brain compared with RA-reared mice on postnatal day 42. Conclusion: Neonatal hyperoxia during the first week of life altered gut microbiota and reduced brain myelination that might associate with the deficits of social interaction and motor coordination in adolescent mice. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Bronchopulmonary dysplasia (BPD) is one of the most common chronic lung diseases in infants, but the ways to prevent and treat BPD are still very limited. We tried to find an effective method for treating BPD by studying the effect of fibroblast growth factor 18 (FGF18) on hyperoxia-induced lung injury in mice. MATERIALS AND METHODS: We placed newborn mice in high-oxygen environment (60-70%) and collected mouse lung tissue for histological examination at 3, 7, 14 and 21 days after birth. The correlation between FGF18 and BPD was studied by analyzing the expression of FGF18 in mouse lung tissue. In addition, we used exogenous FGF18 to stimulate primary mouse type II alveolar epithelial cells (AECs II), and detected changes in oxidative stress, inflammation and NF-κB signaling pathway activity of AECs II to analyze the effects of FGF18 on AECs II. RESULTS: From the 7th day after the birth of the mouse, the lung tissue of the hyperoxia-induced mice suffered significant lung injury relative to the control group. The expression of FGF18 in lung tissue induced by hyperoxia was lower than that in the control group. Cell viability of AECs II stimulated by exogenous FGF18 increased, and FGF18 also reduced oxidative stress and inflammation levels of AECs II and inhibited the AECs II injury caused by hyperoxia. NF-κB signaling pathway activity in hyperoxia-induced lung increased, while exogenous FGF18 could reduce the expression and phosphorylation of NF-κB p65 in AECs II. CONCLUSIONS: Hyperoxia-induced lung injury was accompanied by a decrease in FGF18. FGF18 can reduce oxidative stress and inflammation levels of AECs II by inhibiting the NF-κB signaling pathway, thereby reducing hyperoxia-induced cell injury. [ABSTRACT FROM AUTHOR]

To characterize the institutional oxygen management practices during cardiopulmonary bypass (CPB) in patients undergoing cardiac surgery, including any potential changes during an 8-year study period. A retrospective cohort study. A tertiary care cardiac surgical program. Patients who underwent cardiac surgery involving CPB, with or without hypothermic circulatory arrest (HCA), between January 1, 2010, and December 31, 2017. In addition to baseline patient characteristics, the authors recorded the partial pressures of arterial oxygen (Pa o 2), fraction of inspired oxygen, and mixed venous oxygen saturation during CPB of 696 randomly selected patients during an 8-year study period. The overall mean Pa o 2 was 255 ± 48 mmHg, without any significant change during the 8-year study period (p = 0. 30). The mean Pa o 2 of HCA patients was significantly higher than in patients without HCA (327 ± 93 mmHg v 252 ± 45 mmHg, respectively; p < 0. 001). The current approach to oxygen management during CPB at the authors' institution is within the range of hyperoxemic levels, and these practices have not changed over time. The impact of these practices on patients' outcomes is not fully understood, and additional studies are needed to establish firm evidence to guide optimal oxygen management practice during CPB. [ABSTRACT FROM AUTHOR]

Background: Premature infants often require oxygen (O2) therapy for respiratory distress syndrome; however, excessive use of O2 can cause clinical conditions such as bronchopulmonary dysplasia. Although many treatment methods are currently available, they are not effective in preventing bronchopulmonary dysplasia. Herein, we explored the role of tripartite motif protein 72 (TRIM72), a factor involved in repairing alveolar epithelial wounds, in regulating alveolar cells upon hyperoxia exposure. Methods: In this in vivo study, we used Sprague-Dawley rat pups that were reared in room air or 85% O2 for 2 weeks after birth. The lungs were excised for histological analyses, and TRIM72 expression was assessed on postnatal days 7 and 14. For in vitro experiments, RLE-6TN cells (i.e., rat alveolar type II epithelial cells) and A549 cells (i.e., human lung carcinoma epithelial cells) were exposed to 85% O2 for 5 days. The cells were then analyzed for cell viability, and TRIM72 expression was determined. Results: Exposure to hyperoxia reduced body and lung weight, increased mean linear intercept values, and upregulated TRIM72 expression. In vitro study results revealed increased or decreased lung cell viability upon hyperoxia exposure depending on the suppression or overexpression of TRIM72, respectively. Conclusion: Hyperoxia upregulates TRIM72 expression in neonatal rat lung tissue; moreover, it initiates TRIM72-dependent alveolar epithelial cell death, leading to hyperoxia-induced lung injury. [ABSTRACT FROM AUTHOR]

Oxygen is one of the most commonly used therapies in neonatology but optimum oxygen saturations for preterm infants have been debated for the past 50 years. The history of oxygen use in this population and multiple clinical trials over the years have shown that liberal oxygen administration is associated with retinopathy of prematurity (ROP) and bronchopulmonary dysplasia (BPD) whereas restrictive use results in increased mortality and neurodisability. Pulse oximetry (SpO 2) is a bedside tool to guide the fraction of inspired oxygen (FiO 2) delivered to the patient, and is the current standard of care for continuous monitoring. Although evidence favours targeting predetermined oxygen saturation ranges, achieving this goal consistently in clinical practice has been challenging due to intrinsic pulmonary immaturity, the need for respiratory support therapies and factors relating to the bedside caregivers ability to adjust FiO 2. This review article focuses on the difficulties of titrating oxygen therapy in this vulnerable group and provides recommendations for the best practice based on up to date evidence. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that inflammation plays an important role in the occurrence and development of bronchopulmonary dysplasia (BPD); however, there were rare researches about the changes of neutrophils and their influence on the prognosis of BPD. Hence, we aimed to explore the changes in the number of peripheral blood neutrophils (PBNs), and the relationship between these changes and susceptibility to pulmonary infection among children with BPD. Firstly, the gene expression of lung tissues and the number of PBNs were respectively detected by RNA sequencing and complete blood count in the 85% O 2 -induced BPD model rats. Then it was analyzed the number of PBNs after birth and the incidence of pneumonia within 6 months of corrected age (CA) after discharge among full-term infants (FTIs: gestational age [GA] between 370/7 and 416/7 weeks, n = 88), preterm infants with (PTIs-BPD: GA <32 weeks, n = 35) or without BPD (PTIs-nBPD: GA <32 weeks, n = 41). The levels of S100A8 and S100A9 mRNAs were significantly decreased in the lungs of BPD rats. Moreover, the number of PBNs was also decreased in BPD rats. The number of PBNs at birth in FTIs was significantly greater than that in PTIs-BPD or in PTIs-nBPD (p < 0.001), while those between PTIs-BPD and PTIs-nBPD showed no significant difference (p > 0.05). Although the peripheral blood neutrophils decreased overall after birth in both PTIs-nBPD and PTIs-BPD groups, only the reduction in the PTIs-BPD group was significant (p < 0.001). Importantly, at 36–37 weeks of postmenstrual age (PMA), the number of PBNs in PTIs-BPD was significantly fewer than that in PTIs-nBPD (p < 0.001). In addition, PTIs-BPD had a significantly higher incidence of pneumonia than PTIs-nBPD within 6 months of CA after discharge (p < 0.01). The number of PBNs in PTIs-BPD decreased progressively when compared to that in PTIs-nBPD, which might contribute to their susceptibility to pulmonary infection. [ABSTRACT FROM AUTHOR]

Objective: Brief early administration of supplemental oxygen (sO2) to create hyperoxia may increase oxygenation to penumbral tissue and improve stroke outcomes. Hyperoxia may also result in respiratory compromise and vasoconstriction leading to worse outcomes. This study examines the effects of prehospital sO2 in stroke.Methods: This is a retrospective analysis of adult acute stroke patients (aged ≥18 years) presenting via EMS to an academic Comprehensive Stroke Center between January 1, 2013 and December 31, 2017. Demographic and clinical characteristics obtained from Get with the Guidelines-Stroke registry and subjects' medical records were compared across three groups based on prehospital oxygen saturation and sO2 administration. Chi-square, ANOVA, and multivariate logistic regression were used to determine if sO2 status was associated with neurological outcomes or respiratory complications.Results: 1352 eligible patients were identified. 62.7% (n = 848) did not receive sO2 ("controls"), 10.7% (n = 144) received sO2 due to hypoxia ("hypoxia"), and 26.6% (n = 360) received sO2 despite normoxia ("hyperoxia"). The groups represented a continuum from more severe deficits (hypoxia) to less severe deficits (controls): mean prehospital GCS (hypoxia -12, hyperoxia - 2, controls - 14 p ≤ 0.001), mean initial NIHSS (hypoxia - 15, hyperoxia - 13, controls - 8 p < 0.001). After controlling for potential confounders, all groups had similar rates of respiratory complications and favorable neurological outcomes.Conclusions: Hyperoxic subjects had no significant increase in respiratory complications, nor did they differ in neurologic outcomes at discharge when controlling for confounders. While limited by the retrospective nature, this suggests brief, early sO2 for stroke may be safe to evaluate prospectively. [ABSTRACT FROM AUTHOR]

BACKGROUND: Patients undergoing mechanical ventilation in the ICU often receive supplemental oxygen. If not closely monitored, this may lead to hyperoxia. The use of an oxygen-weaning protocol may reduce this risk by pacing the titration of oxygen therapy to patient needs. ICU protocols are correlated with decreased mortality and length of stay and have great potential for cost savings. The goals of this study were to determine whether the oxygen-weaning protocol at a university-affiliated hospital was followed and to measure the length of time respiratory therapists took to wean patients once the oxygen-weaning parameters were met. METHODS: This was a retrospective chart review of subjects > 18 y of age admitted to the medical ICU who underwent intubation and mechanical ventilation and were placed on an oxygen therapy protocol. The following data were collected: demographics, arterial blood gases, the length of time to change FIO2 after meeting weaning parameters, and the percent change in FIO2. RESULTS: Data were collected from 30 subjects. The most common oxygen saturation parameter measured via pulse oximetry (SpO2) used to initiate weaning oxygen was 92%. The mean 6 SD FIO2 administered to subjects was 39.6 6 15.3% prior to extubation. The majority of subjects exhibited adequate oxygenation prior to extubation (mean 6 SD): PaO2 99.3 6 6.7 mm Hg, SaO2 95.1 6 26.9%. The mean 6 SD length of time to the first change in FIO2 from the time a subject met the weaning criteria was 9.1 6 10.6 h (range 1- 39 h; interquartile range 2-13 h). CONCLUSIONS: Subjects admitted to the medical ICU who were intubated, mechanically ventilated, and placed on the oxygen therapy protocol experienced a significant delay in oxygen weaning. Closer monitoring and adherence to the oxygen-weaning protocol should be considered to reduce the potential risk for hyperoxia. [ABSTRACT FROM AUTHOR]

Objective: Hyperoxia, the delivery of high levels of supplemental oxygen (sO2) despite normoxia, may increase cerebral oxygenation to penumbral tissue and improve stroke outcomes. However, it may also alter peripheral hemodynamic profiles with potential negative effects on cerebral blood flow (CBF). This study examines the hemodynamic consequences of prehospital sO2 in stroke.Methods: A retrospective analysis of adult acute stroke patients (aged ≥18 years) presenting via EMS to an academic Comprehensive Stroke Center between January 1, 2013 and December 31, 2017 was conducted using demographic and clinical characteristics obtained from Get with the Guidelines-Stroke registry and subjects' medical records. Outcomes were compared across three groups based on prehospital oxygen saturation and sO2 administration. Chi-square, ANOVA, and multivariable linear regression were used to determine if sO2 was associated with differences in peripheral hemodynamic profiles.Results: All subjects had similar initial EMS vitals except for oxygen saturation. However, both univariate and multivariable analysis revealed that hyperoxia subjects had slightly lower average ED mean arterial pressures (MAP) compared to normoxia (Cohen's d = 0.313).Conclusions: Prehospital-initiated hyperoxia for acute stroke is associated with a small, but significant decrease in average ED MAP, without changes in heart rate, compared to normoxia. While limited by the inability to link changes in peripheral hemodynamical profiles directly to changes in CBF, this study suggests that hyperoxia may result in a relative hypotension. Further studies are needed to determine if this small change in peripheral vascular resistance translates into a clinically significant reduced CBF. [ABSTRACT FROM AUTHOR]