-
Revue Des Maladies Respiratoires Sep 2022Although standard oxygen is the first-line therapy in patients with acute hypoxemic respiratory failure, high-flow nasal oxygen has gained major popularity in ICUs due... (Review)
Review
Although standard oxygen is the first-line therapy in patients with acute hypoxemic respiratory failure, high-flow nasal oxygen has gained major popularity in ICUs due to its simplicity of application, good comfort for patients, and efficiency in improving oxygenation. Physiological effects of high-flow oxygen therapy can limit the physiological consequences of acute hypoxemic respiratory failure and may mitigate the deleterious effects of high and prolonged inspiratory efforts generated by patients. Although clinical studies have reported a decreased risk of intubation with high-flow oxygen therapy as compared with conventional oxygen therapy, its benefits with regard to survival are uncertain. However, a more precise definition of acute hypoxemic respiratory failure including a classification of severity levels based on oxygenation levels is needed, the objective being to better compare the efficiency of different non-invasive oxygenation supports (conventional oxygen therapy, high-flow oxygen and non-invasive ventilation). Moreover, other clinical trials are needed to confirm the place and the benefit of these oxygenation supports, particularly high-flow nasal oxygen therapy, in acute hypoxemic respiratory failure, especially in the severe forms.
Topics: Humans; Hypoxia; Noninvasive Ventilation; Oxygen; Oxygen Inhalation Therapy; Respiratory Insufficiency
PubMed: 35918276
DOI: 10.1016/j.rmr.2022.06.001 -
European Journal of Pharmacology Nov 2023High-altitude pulmonary edema (HAPE) is a potentially fatal disease. Notoginsenoside R1 is a novel phytoestrogen with anti-inflammatory, antioxidant and anti-apoptosis...
High-altitude pulmonary edema (HAPE) is a potentially fatal disease. Notoginsenoside R1 is a novel phytoestrogen with anti-inflammatory, antioxidant and anti-apoptosis properties. However, its effects and underlying mechanisms in the protection of hypobaric hypoxia-induced HAPE rats remains unclear. This study aimed to explore the protective effects and underlying mechanisms of Notoginsenoside R1 in hypobaric hypoxia-induced HAPE. We found that Notoginsenoside R1 alleviated the lung tissue injury, decreased lung wet/dry ratio, and reduced inflammation and oxidative stress. Additionally, Notoginsenoside R1 ameliorated the changes in arterial blood gas, decreased the total protein concentration in bronchoalveolar lavage fluid, and inhibited the occurrence of apoptosis caused by HAPE. In the process of further exploration of the mechanism, it was found that Notoginsenoside R1 could promote the activation of ERK1/2-P90rsk-BAD signaling pathway, and the effect of Notoginsenoside R1 was attenuated after the use of ERK1/2 inhibitor U0126. Our study indicated that the protective effects of Notoginsenoside R1 against HAPE were mainly related to the inhibition of inflammation, oxidative stress, and apoptosis. Notoginsenoside R1 may be a potential candidate for preventing HAPE.
Topics: Rats; Animals; Altitude; MAP Kinase Signaling System; Pulmonary Edema; Hypoxia; Inflammation
PubMed: 37775017
DOI: 10.1016/j.ejphar.2023.176065 -
Comparative Biochemistry and... Sep 2022Reactive oxygen species (ROS) are important cellular signalling molecules but sudden changes in redox balance can be deleterious to cells and lethal to the whole... (Review)
Review
Reactive oxygen species (ROS) are important cellular signalling molecules but sudden changes in redox balance can be deleterious to cells and lethal to the whole organism. ROS production is inherently linked to environmental oxygen availability and many species live in variable oxygen environments that can range in both severity and duration of hypoxic exposure. Given the importance of redox homeostasis to cell and animal viability, it is not surprising that early studies in species adapted to various hypoxic niches have revealed diverse strategies to limit or mitigate deleterious ROS changes. Although research in this area is in its infancy, patterns are beginning to emerge in the suites of adaptations to different hypoxic environments. This review focuses on redox adaptations (i.e., modifications of ROS production and scavenging, and mitigation of oxidative damage) in hypoxia-tolerant vertebrates across a range of hypoxic environments. In general, evidence suggests that animals adapted to chronic lifelong hypoxia are in homeostasis, and do not encounter major oxidative challenges in their homeostatic environment, whereas animals exposed to seasonal chronic anoxia or hypoxia rapidly downregulate redox balance to match a hypometabolic state and employ robust scavenging pathways during seasonal reoxygenation. Conversely, animals adapted to intermittent hypoxia exposure face the greatest degree of ROS imbalance and likely exhibit enhanced ROS-mitigation strategies. Although some progress has been made, research in this field is patchy and further elucidation of mechanisms that are protective against environmental redox challenges is imperative for a more holistic understanding of how animals survive hypoxic environments.
Topics: Animals; Hypoxia; Oxidation-Reduction; Oxidative Stress; Oxygen; Reactive Oxygen Species; Vertebrates
PubMed: 35724954
DOI: 10.1016/j.cbpa.2022.111259 -
American Journal of Respiratory and... Apr 2023
Topics: Infant; Infant, Newborn; Humans; Infant, Premature; Bronchopulmonary Dysplasia; Hypertension, Pulmonary; Hypoxia; Oxygen; Respiration Disorders
PubMed: 36630576
DOI: 10.1164/rccm.202212-2290ED -
International Journal of Developmental... Dec 2021Neonatal anoxia is a well-known world health problem that results in neurodevelopmental deficits, such as sensory alterations that are observed in patients with cerebral...
Neonatal anoxia is a well-known world health problem that results in neurodevelopmental deficits, such as sensory alterations that are observed in patients with cerebral palsy and autism disorder, for which oxygen deprivation is a risk factor. Nociceptive response, as part of the sensory system, has been reported as altered in these patients. To determine whether neonatal oxygen deprivation alters nociceptive sensitivity and promotes medium- and long-term inflammatory feedback in the central nervous system, Wistar rats of around 30 h old were submitted to anoxia (100% nitrogen flux for 25 min) and evaluated on PND23 (postpartum day) and PND90. The nociceptive response was assessed by mechanical, thermal, and tactile tests in the early postnatal and adulthood periods. The lumbar spinal cord (SC, L4-L6) motor neurons (MNs) and the posterior insular cortex neurons were counted and compared with their respective controls after anoxia. In addition, we evaluated the possible effect of anoxia on the expression of astrocytes in the SC at adulthood. The results showed increased nociceptive responses in both males and females submitted to anoxia, although these responses were different according to the nociceptive stimulus. A decrease in MNs in adult anoxiated females and an upregulation of GFAP expression in the SC were observed. In the insular cortex, a decrease in the number of cells of anoxiated males was observed in the neonatal period. Our findings suggest that oxygen-deprived nervous systems in rats may affect their response at the sensorimotor pathways and respective controlling centers with sex differences, which were related to the used stimulus.
Topics: Animals; Female; Hypoxia; Insular Cortex; Male; Neurons; Nociception; Rats; Rats, Wistar; Sex Factors; Spinal Cord
PubMed: 34342028
DOI: 10.1002/jdn.10145 -
International Journal of Medical... 2023Severe hypoxia can induce a range of systemic disorders; however, surprising resilience can be obtained through sublethal adaptation to hypoxia, a process termed as... (Review)
Review
Severe hypoxia can induce a range of systemic disorders; however, surprising resilience can be obtained through sublethal adaptation to hypoxia, a process termed as hypoxic conditioning. A particular form of this strategy, known as intermittent hypoxia conditioning hormesis, alternates exposure to hypoxic and normoxic conditions, facilitating adaptation to reduced oxygen availability. This technique, originally employed in sports and high-altitude medicine, has shown promise in multiple pathologies when applied with calibrated mild to moderate hypoxia and appropriate hypoxic cycles. Recent studies have extensively investigated the protective role of intermittent hypoxia conditioning and its underlying mechanisms using animal models, demonstrating its potential in organ protection. This involves a range of processes such as reduction of oxidative stress, inflammation, and apoptosis, along with enhancement of hypoxic gene expression, among others. Given that intermittent hypoxia conditioning fosters beneficial physiological responses across multiple organs and systems, this review presents a comprehensive analysis of existing studies on intermittent hypoxia and its potential advantages in various organs. It aims to draw attention to the possibility of clinically applying intermittent hypoxia conditioning as a multi-organ protective strategy. This review comprehensively discusses the protective effects of intermittent hypoxia across multiple systems, outlines potential procedures for implementing intermittent hypoxia, and provides a brief overview of the potential protective mechanisms of intermittent hypoxia.
Topics: Animals; Hypoxia; Oxygen; Oxidative Stress
PubMed: 37859700
DOI: 10.7150/ijms.86622 -
International Journal of Developmental... Apr 2019Neonatal anoxia induces long-term brain injury that may underlie neurobehavioral deficits at adolescence. Neonatal anoxia, induced by exposure of 30-hour old pups to...
Neonatal anoxia induces long-term brain injury that may underlie neurobehavioral deficits at adolescence. Neonatal anoxia, induced by exposure of 30-hour old pups to 100% nitrogen, represents a non-invasive and global stimulus, which simulates clinical conditions of human pre-term babies (around 6 gestational months). Previous studies showed that neonatal anoxia induced impairments of spatial memory and altered anxiety-like behaviors in male rats tested at adult age. This study evaluated if neonatal anoxia induces similar behavioral effects in female rats, as compared to males, by testing the animals at adolescence, and also searched for possible cell losses in hippocampal subfields. Results in the Elevated Plus Maze test showed that anoxic females spent proportionally more time within the open arms as compared to anoxic males, suggesting a less anxious-like behavior. In the Morris Water Maze Test, latencies and path lengths of the anoxic subjects were longer as compared to control subjects, thus indicating that anoxia disrupted the cognitive functions required for spatial mapping. In addition, results showed that anoxia-induced disruption was greater in male rats as compared to female rats. Stereological analysis revealed that anoxic male rats exhibited significant cell losses in the dorsal hippocampus dentate gyrus and CA1 subfields, but not in CA3-2 subfield. Similar results were observed in the ventral hippocampus, but now with cell loss in the male CA3-2 subfield. There were also significant cell loss differences of anoxic male rats as compared to anoxic female rats. In conclusion, neonatal anoxia induces deleterious and long lasting behavioral and cognitive disruptions, and these effects were stronger in male rats as compared to female rats. These changes are congruent with the pattern of cell losses observed in hippocampal subfields. Together, these results emphasize the relevance of scientific research, aiming at clinical strategies and treatments, consider the sex differential patterns of response to neonatal injury.
Topics: Animals; Behavior, Animal; Cell Death; Female; Hippocampus; Hypoxia, Brain; Male; Maze Learning; Rats; Sex Factors; Spatial Memory
PubMed: 30562544
DOI: 10.1016/j.ijdevneu.2018.12.002 -
Annual Review of Entomology Jan 2018Insects can experience functional hypoxia, a situation in which O supply is inadequate to meet oxygen demand. Assessing when functional hypoxia occurs is complex,... (Review)
Review
Insects can experience functional hypoxia, a situation in which O supply is inadequate to meet oxygen demand. Assessing when functional hypoxia occurs is complex, because responses are graded, age and tissue dependent, and compensatory. Here, we compare information gained from metabolomics and transcriptional approaches and by manipulation of the partial pressure of oxygen. Functional hypoxia produces graded damage, including damaged macromolecules and inflammation. Insects respond by compensatory physiological and morphological changes in the tracheal system, metabolic reorganization, and suppression of activity, feeding, and growth. There is evidence for functional hypoxia in eggs, near the end of juvenile instars, and during molting. Functional hypoxia is more likely in species with lower O availability or transport capacities and when O need is great. Functional hypoxia occurs normally during insect development and is a factor in mediating life-history trade-offs.
Topics: Animals; Biological Evolution; Ecosystem; Hypoxia; Insecta; Life Cycle Stages; Oxygen; Temperature
PubMed: 28992421
DOI: 10.1146/annurev-ento-020117-043145 -
Comparative Biochemistry and... May 2022In anoxia-sensitive mammals, hypoxia inducible factor (HIF) promotes cellular survival in hypoxia, but also tumorigenesis. By comparison, anoxia-tolerant vertebrates...
Gene expression of hypoxia-inducible factor (HIF), HIF regulators, and putative HIF targets in ventricle and telencephalon of Trachemys scripta acclimated to 21 °C or 5 °C and exposed to normoxia, anoxia or reoxygenation.
In anoxia-sensitive mammals, hypoxia inducible factor (HIF) promotes cellular survival in hypoxia, but also tumorigenesis. By comparison, anoxia-tolerant vertebrates likely need to circumvent a prolonged upregulation of HIF to survive long-term anoxia, making them attractive biomedical models for investigating HIF regulation. To lend insight into the role of HIF in anoxic Trachemys scripta ventricle and telencephalon, 21 °C- and 5 °C-acclimated turtles were exposed to normoxia, anoxia (24 h at 21 °C; 24 h or 14 d at 5 °C) or anoxia + reoxygenation and the gene expression of HIF-1α (hif1a) and HIF-2α (hif2a), two regulators of HIF, and eleven putative downstream targets of HIF quantified by qPCR. Changes in gene expression with anoxia at 21 °C differentially aligned with a circumvention of HIF activity. Whereas hif1a and hif2a expression was unaffected in ventricle and telencephalon, and BCL2 interacting protein 3 gene expression reduced by 30% in telencephalon, gene expression of vascular endothelial growth factor-A increased in ventricle (4.5-fold) and telencephalon (1.5-fold), and hexokinase 1 (2-fold) and hexokinase 2 (3-fold) gene expression increased in ventricle. At 5 °C, the pattern of gene expression in ventricle or telencephalon was unaltered with oxygenation state. However, cold acclimation in normoxia induced downregulation of HIF-1α, HIF-2α, and HIF target gene expression in telencephalon. Overall, the findings lend support to the postulation that prolonged activation of HIF is counterproductive for long-term anoxia survival. Nevertheless, quantification of the effect of anoxia and acclimation temperature on HIF binding activity and regulation at the protein level are needed to provide a strong scientific framework whereby new strategies for oxygen related pathologies can be developed.
Topics: Acclimatization; Animals; Gene Expression; Hypoxia; Mammals; Telencephalon; Turtles; Vascular Endothelial Growth Factor A
PubMed: 35182763
DOI: 10.1016/j.cbpa.2022.111167 -
Journal of Clinical Pathology May 2021
Topics: Chronic Disease; Female; Fictional Works as Topic; Humans; Hypoxia; Literature, Modern; Male; Medicine in Literature; Pregnancy; Prenatal Exposure Delayed Effects; Teratogens; Tetralogy of Fallot
PubMed: 32763921
DOI: 10.1136/jclinpath-2020-206561