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Background: Cardiac arrest (CA) is a sudden event that is often characterized by hypoxic-ischemic brain injury (HIBI), leading to significant mortality and long-term disability. Brain tissue oxygenation (PbtO2) is an invasive tool for monitoring brain oxygen tension, but it is not routinely used in patients with CA because of the invasiveness and the absence of high-quality data on its effect on outcome. We conducted a systematic review of experimental and clinical evidence to understand the role of PbtO2 in monitoring brain oxygenation in HIBI after CA and the effect of targeted PbtO2 therapy on outcomes. Methods: The search was conducted using four search engines (PubMed, Scopus, Embase, and Cochrane), using the Boolean operator to combine mesh terms such as PbtO2, CA, and HIBI. Results: Among 1,077 records, 22 studies were included (16 experimental studies and six clinical studies). In experimental studies, PbtO2 was mainly adopted to assess the impact of gas exchanges, drugs, or systemic maneuvers on brain oxygenation. In human studies, PbtO2 was rarely used to monitor the brain oxygen tension in patients with CA and HIBI. PbtO2 values had no clear association with patients' outcomes, but in the experimental studies, brain tissue hypoxia was associated with increased inflammation and neuronal damage. Conclusions: Further studies are needed to validate the effect and the threshold of PbtO2 associated with outcome in patients with CA, as well as to understand the physiological mechanisms influencing PbtO2 induced by gas exchanges, drug administration, and changes in body positioning after CA. [ABSTRACT FROM AUTHOR]

Large‐scale shifts in marine species biogeography have been a notable impact of climate change. An effective explanation of what drives these species shifts, as well as accurate predictions of where they might move, is crucial to effectively managing these natural resources and conserving biodiversity. While temperature has been implicated as a major driver of these shifts, physiological processes suggest that oxygen, prey, and other factors should also play important roles. We expanded upon previous temperature‐based distribution models by testing whether oxygen, food web productivity, salinity, and scope for metabolic activity (the Metabolic Index) better explained the changing biogeography of Black Sea Bass (Centropristis striata) in the Northeast US. This species has been expanding further north over the past 15 years. We found that oxygen improved model performance beyond a simple consideration of temperature (ΔAIC = 799, ΔTSS = 0.015), with additional contributions from prey and salinity. However, the Metabolic Index did not substantially increase model performance relative to temperature and oxygen (ΔAIC = 0.63, ΔTSS = 0.0002). Marine species are sensitive to oxygen, and we encourage researchers to use ocean biogeochemical hindcast and forecast products to better understand marine biogeographic changes. [ABSTRACT FROM AUTHOR]

Despite the global ecological importance of climate change, controversy surrounds how oxygen affects the fate of aquatic ectotherms under warming. Disagreements extend to the nature of oxygen bioavailability and whether oxygen usually limits growth under warming, explaining smaller adult size. These controversies affect two influential hypotheses: gill oxygen limitation and oxygen- and capacity-limited thermal tolerance. Here, we promote deeper integration of physiological and evolutionary mechanisms. We first clarify the nature of oxygen bioavailability in water, developing a new mass-transfer model that can be adapted to compare warming impacts on organisms with different respiratory systems and flow regimes. By distinguishing aerobic energy costs of moving oxygen from environment to tissues from costs of all other functions, we predict a decline in energy-dependent fitness during hypoxia despite approximately constant total metabolic rate before reaching critically low environmental oxygen. A new measure of oxygen bioavailability that keeps costs of generating water convection constant predicts a higher thermal sensitivity of oxygen uptake in an amphipod model than do previous oxygen supply indices. More importantly, by incorporating size- and temperature-dependent costs of generating water flow, we propose that oxygen limitation at different body sizes and temperatures can be modeled mechanistically. We then report little evidence for oxygen limitation of growth and adult size under benign warming. Yet occasional oxygen limitation, we argue, may, along with other selective pressures, help maintain adaptive plastic responses to warming. Finally, we discuss how to overcome flaws in a commonly used growth model that undermine predictions of warming impacts. [ABSTRACT FROM AUTHOR]

The scaling of respiratory structures has been hypothesized to be a major driving factor in the evolution of many aspects of animal physiology. Here, we provide the first assessment of the scaling of the spiracles in insects using 10 scarab beetle species differing 180× in mass, including some of the most massive extant insect species. Using X-ray microtomography, we measured the cross-sectional area and depth of all eight spiracles, enabling the calculation of their diffusive and advective capacities. Each of these metrics scaled with geometric isometry. Because diffusive capacities scale with lower slopes than metabolic rates, the largest beetles measured require 10-fold higher PO2 gradients across the spiracles to sustain metabolism by diffusion compared to the smallest species. Large beetles can exchange sufficient oxygen for resting metabolism by diffusion across the spiracles, but not during flight. In contrast, spiracular advective capacities scale similarly or more steeply than metabolic rates, so spiracular advective capacities should match or exceed respiratory demands in the largest beetles. These data illustrate a general principle of gas exchange: scaling of respiratory transport structures with geometric isometry diminishes the potential for diffusive gas exchange but enhances advective capacities; combining such structural scaling with muscle-driven ventilation allows larger animals to achieve high metabolic rates when active. [ABSTRACT FROM AUTHOR]

During the period of use of hyperbaric oxygen (HBO2) in medical treatment and in scuba diving, extensive knowledge has been accumulated about the mechanisms of its biological action. In the present work, we analyze the experimental data of recent years related to the cellular and molecular mechanisms of the physiological and neurotoxic effects of hyperbaric oxygen. New data on the physiological action of HBO2 concern the mechanisms of hyperoxic vasoconstriction and baroreflex activation in hyperoxia. The toxic effect of hyperbaric oxygen is realized through the intensive production of reactive oxygen and nitrogen species, which cause post-translational modification of proteins responsible for neuronal electrogenesis and synaptic transmission in the GABAergic system of the brain. [ABSTRACT FROM AUTHOR]

Significance: The role of reactive oxygen/nitrogen species as "friend" or "foe" messengers in the whole body is well characterized. Depending on the concentration in the tissue considered, these molecular actors exert beneficial or deleterious impacts leading to a pathological state, as observed in metabolic disorders such as type 2 diabetes and obesity. Recent Advances: Among the tissues impacted by oxidation and inflammation in this pathological state, the intestine is a site of dysfunction that can establish diabetic symptoms, such as alterations in the intestinal barrier, gut motility, microbiota composition, and gut/brain axis communication. In the intestine, reactive oxygen/nitrogen species (from the host and/or microbiota) are key factors that modulate the transition from physiological to pathological signaling. Critical Issues: Controlling the levels of intestinal reactive oxygen/nitrogen species is a complicated balance between positive and negative impacts that is in constant equilibrium. Here, we describe the synthesis and degradation of intestinal reactive oxygen/nitrogen species and their interactions with the host. The development of novel redox-based therapeutics that alter these processes could restore intestinal health in patients with metabolic disorders. Future Directions: Deciphering the mode of action of reactive oxygen/nitrogen species in the gut of obese/diabetic patients could result in a future therapeutic strategy that combines nutritional and pharmacological approaches. Consequently, preventive and curative treatments must take into account one of the first sites of oxidative and inflammatory dysfunctions in the body, that is, the intestine. Antioxid. Redox Signal. 37, 394–415. [ABSTRACT FROM AUTHOR]

In general anaesthesia, early collapse of poorly ventilated lung segments with low alveolar ventilation-perfusion ratios occurs and may lead to postoperative pulmonary complications after abdominal surgery. An 'open lung' ventilation strategy involves lung recruitment followed by 'individualised' positive end-expiratory pressure titrated to maintain recruitment of low alveolar ventilation-perfusion ratio lung segments. There are limited data in laparoscopic surgery on the effects of this on pulmonary gas exchange. Forty laparoscopic bowel surgery patients were randomly assigned to standard ventilation or an 'open lung' ventilation intervention, with end-tidal target sevoflurane of 1% supplemented by propofol infusion. After peritoneal insufflation, stepped lung recruitment was performed in the intervention group followed by maintenance positive end-expiratory pressure of 12-15 cmH2O adjusted to maintain dynamic lung compliance at post-recruitment levels. Baseline gas and blood samples were taken and repeated after a minimum of 30 minutes for oxygen and carbon dioxide and for sevoflurane partial pressures using headspace equilibration. The sevoflurane arterial/alveolar partial pressure ratio and alveolar deadspace fraction were unchanged from baseline and remained similar between groups (mean (standard deviation) control group = 0.754 (0.086) versus intervention group = 0.785 (0.099), P = 0.319), while the arterial oxygen partial pressure/fractional inspired oxygen concentration ratio was significantly higher in the intervention group at the second timepoint (control group median (interquartile range) 288 (234-372) versus 376 (297-470) mmHg in the intervention group, P = 0.011). There was no difference between groups in the sevoflurane consumption rate. The efficiency of sevoflurane uptake is not improved by open lung ventilation in laparoscopy, despite improved arterial oxygenation associated with effective and sustained recruitment of low alveolar ventilation-perfusion ratio lung segments. [ABSTRACT FROM AUTHOR]

The light-absorbing retina has an exceptionally high oxygen demand, which imposes two conflicting needs: high rates of blood perfusion and an unobstructed light path devoid of blood vessels. This review discusses mechanisms and physiological trade-offs underlying retinal oxygen supply in vertebrates and examines how these physiological systems supported the evolution of vision. [ABSTRACT FROM AUTHOR]

As blood flows from the portal triad to the central vein, cell-mediated depletion establishes gradients of soluble factors such as oxygen, nutrients, and hormones, which act through molecular pathways (e.g., Wnt/β-catenin, hedgehog) to spatially regulate hepatocyte functions along the sinusoid. Such "zonation" can lead to the compartmentalized initiation of several liver diseases, including alcoholic/non-alcoholic fatty liver diseases, chemical/drug-induced toxicity, and hepatocellular carcinoma, and can also modulate liver regeneration. Transgenic rodent models provide valuable information on the key molecular regulators of zonation, while in vitro models allow for subjecting cells to precisely controlled factor gradients and elucidating species–specific differences in zonation. Here, we discuss the latest advances in both in vivo and in vitro models of liver zonation and pending questions to be addressed moving forward. Ultimately, obtaining a deeper understanding of zonation can lead to the development of more effective therapeutics for liver diseases, microphysiological systems, and scalable cell-based therapies. [ABSTRACT FROM AUTHOR]

In mammals, physiology and metabolism are shaped both by immediate and anticipatory responses to environmental changes through the myriad of molecular mechanisms. Whilst the former is mostly mediated through different acute signalling pathways the latter is primarily orchestrated by the circadian clock. Oxygen is vital for life and as such mammals have evolved different mechanisms to cope with changes in oxygen levels. It is widely accepted that oxygen sensing through the HIF‐1 signalling pathway is paramount for the acute response to changes in oxygen levels. Circadian clocks are molecular oscillators that control 24 hours rhythms in various aspects of physiology and behaviour. Evidence emerging in recent years points towards pervasive molecular and functional interactions between these two pathways on multiple levels. Daily oscillations in oxygen levels are circadian clock‐controlled and can reset the clock through HIF‐1. Furthermore, the circadian clock appears to modulate the hypoxic response. We review herein the literature related to the crosstalk between the circadian clockwork and the oxygen‐signalling pathway in mammals at the molecular and physiological level both under normal and pathologic conditions. [ABSTRACT FROM AUTHOR]

Hypoxic aquatic environments occur more frequently as a result of climate change, thereby exerting challenges on the physiological and metabolic functions of aquatic animals. In this study, a model fish, zebrafish (Danio rerio) was used to observe the climate-induced hypoxic effect on the upper thermal limit (critical thermal maximum; CTmax), hemoglobin, and blood glucose levels, and abnormalities of erythrocytes at cellular and nuclear level. The value of CTmax decreased significantly under hypoxia (39.10 ± 0.96 °C) compared to normoxia (43.70 ± 0.91 °C). At CTmax, hemoglobin levels were much lower (9.33 ± 0.60 g/dL) and blood glucose levels were significantly higher (194.20 ± 11.33 mg/L) under hypoxia than they were under normoxia and at the beginning of the experiment. Increased frequencies of abnormalities in the erythrocytes at both cellular (fusion, twin, elongated, spindle and tear drop shaped) and nuclear (micronucleus, karyopyknosis, binuclei, nuclear degeneration and notched nuclei) levels were also found under hypoxia compared to normoxia. These results suggest that hypoxic conditions significantly alter the temperature tolerance and subsequent physiology in zebrafish. Our findings will aid in the development of effective management techniques for aquatic environments with minimum oxygen availability. • Hypoxic condition alters the temperature tolerance physiology in zebrafish. • Hypoxic condition negatively influences hemoglobin and blood glucose levels. • There are increased abnormalities in the erythrocytes at both cellular and nuclear levels. [ABSTRACT FROM AUTHOR]

• Intron retention is a mechanism of erythropoietin regulation in response to ischemia in brain cells. • Intron retention shows a temporal effect in brain cells. • Intron retention in EPO is a deliberate physiological mechanism of post-transcriptional regulation. Intron retention is a mechanism of post-transcriptional gene regulation, including genes involved in erythropoiesis. Erythropoietin (EPO) is a hormone without evidence of intracellular vesicle storage that regulates erythropoiesis. We hypothesize that EPO uses intron retention as a mechanism of post-transcriptional regulation in response to hypoxia and ischemia. Cell models of hypoxia and ischemia for kidney, liver, and brain cells were examined for intron retention by real time quantitative PCR. EPO expression increased in most cells except for blood brain barrier and liver cells. The intron retained transcript ratio decreased in brain cells, except for Astrocytes, but showed no change in kidney or liver after 24 h of ischemia. The shift in intron ratio was maintained when using poly (A) enriched cDNA, suggesting that intron retention is not due to immature transcripts. The expression of EPO was elevated at variable time points amongst cell models with the intron ratio also changing over a time course of 2 to 16 h after ischemia. We conclude that intron retention is a mechanism regulating EPO expression in response to ischemia in a tissue specific manner. [ABSTRACT FROM AUTHOR]

Objective: Some proposals for oxygen uptake plateau identification are based on linear regression adaptations. However, linear regression does not adequately explain the oxygen uptake nonlinear dynamics. Recently, segmented regression was considered as an alternative to fit this dynamics, by performing an approximation by straight line segments, which provided a satisfactory fit. In this context, the non-plateau and plateau hypotheses were verified by means of a Wald-type test. This work aims to extend these proposals to scenarios with autocorrelated data. Methods: We propose an algorithm to estimate the segmented regression model under autocorrelation using generalized least squares and suggest a bootstrap method to resample from the null distribution of Wald’s statistic. The performance of the estimate and methods of the plateau diagnosis were evaluated via Monte Carlo experiments. Results: The empirical results show that, under autocorrelation, the proposed estimator performs better when compared to the classic method, mainly in scenarios with small sample sizes and moderate/strong autocorrelation structure. The simulations also showed that the plateau diagnosis test has a coherent empirical Type 1 Error probability and good power. Conclusion: We proposed an alternative to estimate the parameters of a segmented regression model for autocorrelated data and an oxygen consumption plateau bootstrap test, and concluded the methods present good performance under simulated and applied case studies. Significance: The proposed method was used to model real oxygen consumption data. Empirical evidence shows that the methods can be used to objectively identify the plateau in oxygen consumption only by specifying a tolerable significance level. [ABSTRACT FROM AUTHOR]