An abnormal increase in the amount of oxygen in the tissues and organs.
An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.
Small polyhedral outpouchings along the walls of the alveolar sacs, alveolar ducts and terminal bronchioles through the walls of which gas exchange between alveolar air and pulmonary capillary blood takes place.
The therapeutic intermittent administration of oxygen in a chamber at greater than sea-level atmospheric pressures (three atmospheres). It is considered effective treatment for air and gas embolisms, smoke inhalation, acute carbon monoxide poisoning, caisson disease, clostridial gangrene, etc. (From Segen, Dictionary of Modern Medicine, 1992). The list of treatment modalities includes stroke.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
Refers to animals in the period of time just after birth.
Relatively complete absence of oxygen in one or more tissues.
A small cluster of chemoreceptive and supporting cells located near the bifurcation of the internal carotid artery. The carotid body, which is richly supplied with fenestrated capillaries, senses the pH, carbon dioxide, and oxygen concentrations in the blood and plays a crucial role in their homeostatic control.
The pressure that would be exerted by one component of a mixture of gases if it were present alone in a container. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Cells specialized to detect chemical substances and relay that information centrally in the nervous system. Chemoreceptor cells may monitor external stimuli, as in TASTE and OLFACTION, or internal stimuli, such as the concentrations of OXYGEN and CARBON DIOXIDE in the blood.
Damage to any compartment of the lung caused by physical, chemical, or biological agents which characteristically elicit inflammatory reaction. These inflammatory reactions can either be acute and dominated by NEUTROPHILS, or chronic and dominated by LYMPHOCYTES and MACROPHAGES.
Electrodes which can be used to measure the concentration of particular ions in cells, tissues, or solutions.
The blood vessels which supply and drain the RETINA.
A chronic lung disease developed after OXYGEN INHALATION THERAPY or mechanical ventilation (VENTILATION, MECHANICAL) usually occurring in certain premature infants (INFANT, PREMATURE) or newborn infants with respiratory distress syndrome (RESPIRATORY DISTRESS SYNDROME, NEWBORN). Histologically, it is characterized by the unusual abnormalities of the bronchioles, such as METAPLASIA, decrease in alveolar number, and formation of CYSTS.
A bilateral retinopathy occurring in premature infants treated with excessively high concentrations of oxygen, characterized by vascular dilatation, proliferation, and tortuosity, edema, and retinal detachment, with ultimate conversion of the retina into a fibrous mass that can be seen as a dense retrolental membrane. Usually growth of the eye is arrested and may result in microophthalmia, and blindness may occur. (Dorland, 27th ed)
Epithelial cells that line the PULMONARY ALVEOLI.
A scanning probe microscopy technique that uses an ultramicroelectrode as the scanning probe that simultaneously records changes in electrochemical potential as it scans thereby creating topographical images with localized electrochemical information.
A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
Measurement of oxygen and carbon dioxide in the blood.
Inhalation of oxygen aimed at restoring toward normal any pathophysiologic alterations of gas exchange in the cardiopulmonary system, as by the use of a respirator, nasal catheter, tent, chamber, or mask. (From Dorland, 27th ed & Stedman, 25th ed)
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood.
The act of breathing with the LUNGS, consisting of INHALATION, or the taking into the lungs of the ambient air, and of EXHALATION, or the expelling of the modified air which contains more CARBON DIOXIDE than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= OXYGEN CONSUMPTION) or cell respiration (= CELL RESPIRATION).
The physical or mechanical action of the LUNGS; DIAPHRAGM; RIBS; and CHEST WALL during respiration. It includes airflow, lung volume, neural and reflex controls, mechanoreceptors, breathing patterns, etc.
The mixture of gases present in the earth's atmosphere consisting of oxygen, nitrogen, carbon dioxide, and small amounts of other gases.
A pulmonary surfactant associated protein that plays a role in alveolar stability by lowering the surface tension at the air-liquid interface. It is a membrane-bound protein that constitutes 1-2% of the pulmonary surfactant mass. Pulmonary surfactant-associated protein C is one of the most hydrophobic peptides yet isolated and contains an alpha-helical domain with a central poly-valine segment that binds to phospholipid bilayers.

Hyperoxia induces the neuronal differentiated phenotype of PC12 cells via a sustained activity of mitogen-activated protein kinase induced by Bcl-2. (1/953)

We previously reported that rat pheochromocytoma PC12 cells express the neuronal differentiated phenotype under hyperoxia through the production of reactive oxygen species (ROS). In the present study, we found that in this phenotype, Bcl-2, an apoptosis inhibitor, affects mitogen-activated protein (MAP)-kinase activity, which is known as a key enzyme of the signal-transduction cascade for differentiation. When PC12 cells were cultured under hyperoxia, a rapid increase in MAP-kinase activity, including that of both p42 and p44, was observed. Although the activity level then decreased quickly, activity higher than the control level was observed for 48 h. PD98059, an inhibitor of MAP kinase, suppressed the hyperoxia-induced neurite extensions, suggesting the involvement of MAP-kinase activity in the mechanism of differentiation induced by ROS. An elevation of Bcl-2 expression was observed after culturing PC12 cells for 24 h under hyperoxia. This Bcl-2 elevation was not affected by treatment with PD98059, suggesting that it did not directly induce neurite extension under hyperoxia. However, the blockade of the Bcl-2 elevation by an antisense oligonucleotide inhibited the sustained MAP-kinase activity and neurite extensions under hyperoxia. Further, in PC12 cells highly expressing Bcl-2, the sustained MAP-kinase activity and neurite extensions under hyperoxia were enhanced. These results suggested that MAP kinase is activated through the production of ROS, and the subsequent elevation of Bcl-2 expression sustains the MAP-kinase activity, resulting in the induction of the neuronal-differentiation phenotype of PC12 cells under hyperoxia.  (+info)

Effect of hyperoxia on human macrophage cytokine response. (2/953)

In the development of lung damage induced by oxidative stress, it has been proposed that changes in alveolar macrophages (AM) function with modifications in cytokine production may contribute to altered repair processes. To characterize the changes in profiles of cytokine production by macrophages exposed to oxidants, the effects of hyperoxia (95% O2) on interleukin (IL)-1 beta, IL-6, IL-8, and tumour necrosis factor-alpha (TNF-alpha) expression were studied. Experiments were first performed using AM obtained from control subjects and children with interstitial lung disease. Results showed that a 48 h O2 exposure was associated with two distinct patterns of response: a decrease in TNF-alpha, IL-1 beta and IL-6 expression, and an increase in IL-8. To complete these observations we used U937 cells that were exposed for various durations to hyperoxia. We confirmed that a 48 h O2 exposure led to similar changes with a decrease in TNF-alpha, IL-1 beta and IL-6 production and an increase in IL-8. Interestingly, this cytokine response was preceded during the first hours of O2 treatment by induction of TNF-alpha, IL-1 beta and IL-6. These data indicate that hyperoxia induces changes in the expression of macrophages inflammatory cytokines, and that these modifications appear to be influenced by the duration of O2 exposure.  (+info)

Exposure to hyperoxia decreases the expression of vascular endothelial growth factor and its receptors in adult rat lungs. (3/953)

Exposure to high levels of inspired oxygen leads to respiratory failure and death in many animal models. Endothelial cell death is an early finding, before the onset of respiratory failure. Vascular endothelial growth factor (VEGF) is highly expressed in the lungs of adult animals. In the present study, adult Sprague-Dawley rats were exposed to >95% FiO2 for 24 or 48 hours. Northern blot analysis revealed a marked reduction in VEGF mRNA abundance by 24 hours, which decreased to less than 50% of control by 48 hours. In situ hybridization revealed that VEGF was highly expressed in distal airway epithelial cells in controls but disappeared in the oxygen-exposed animals. Immunohistochemistry and Western blot analyses demonstrated that VEGF protein was decreased at 48 hours. TUNEL staining demonstrated the presence of apoptotic cells coincident with the decline in VEGF. Abundance of VEGF receptor mRNAs (Flt-1 and KDR/Flk) decreased in the late time points of the study (48 hours), possibly secondary to the loss of endothelial cells. We speculate that VEGF functions as a survival factor in the normal adult rat lung, and its loss during hyperoxia contributes to the pathophysiology of oxygen-induced lung damage.  (+info)

Exogenous administration of heme oxygenase-1 by gene transfer provides protection against hyperoxia-induced lung injury. (4/953)

Heme oxygenase-1 (HO-1) confers protection against a variety of oxidant-induced cell and tissue injury. In this study, we examined whether exogenous administration of HO-1 by gene transfer could also confer protection. We first demonstrated the feasibility of overexpressing HO-1 in the lung by gene transfer. A fragment of the rat HO-1 cDNA clone containing the entire coding region was cloned into plasmid pAC-CMVpLpA, and recombinant adenoviruses containing the rat HO-1 cDNA fragment Ad5-HO-1 were generated by homologous recombination. Intratracheal administration of Ad5-HO-1 resulted in a time-dependent increase in expression of HO-1 mRNA and protein in the rat lungs. Increased HO-1 protein expression was detected diffusely in the bronchiolar epithelium of rats receiving Ad5-HO-1, as assessed by immunohistochemical studies. We then examined whether ectopic expression of HO-1 could confer protection against hyperoxia-induced lung injury. Rats receiving Ad5-HO-1, but not AdV-betaGal, a recombinant adenovirus expressing Escherichia coli beta-galactosidase, before exposure to hyperoxia (>99% O2) exhibited marked reduction in lung injury, as assessed by volume of pleural effusion and histological analyses (significant reduction of edema, hemorrhage, and inflammation). In addition, rats receiving Ad5-HO-1 also exhibited increased survivability against hyperoxic stress when compared with rats receiving AdV-betaGal. Expression of the antioxidant enzymes manganese superoxide dismutase (Mn-SOD) and copper-zinc superoxide dismutase (CuZn-SOD) and of L-ferritin and H-ferritin was not affected by Ad5-HO-1 administration. Furthermore, rats treated with Ad5-HO-1 exhibited attenuation of hyperoxia-induced neutrophil inflammation and apoptosis. Taken together, these data suggest the feasibility of high-level HO-1 expression in the rat lung by gene delivery. To our knowledge, we have demonstrated for the first time that HO-1 can provide protection against hyperoxia-induced lung injury in vivo by modulation of neutrophil inflammation and lung apoptosis.  (+info)

Extracellular superoxide dismutase in the airways of transgenic mice reduces inflammation and attenuates lung toxicity following hyperoxia. (5/953)

Extracellular superoxide dismutase (EC-SOD, or SOD3) is the major extracellular antioxidant enzyme in the lung. To study the biologic role of EC-SOD in hyperoxic-induced pulmonary disease, we created transgenic (Tg) mice that specifically target overexpression of human EC-SOD (hEC-SOD) to alveolar type II and nonciliated bronchial epithelial cells. Mice heterozygous for the hEC-SOD transgene showed threefold higher EC-SOD levels in the lung compared with wild-type (Wt) littermate controls. A significant amount of hEC-SOD was present in the epithelial lining fluid layer. Both Tg and Wt mice were exposed to normobaric hyperoxia (>99% oxygen) for 48, 72, and 84 hours. Mice overexpressing hEC-SOD in the airways attenuated the hyperoxic lung injury response, showed decreased morphologic evidence of lung damage, had reduced numbers of recruited inflammatory cells, and had a reduced lung wet/dry ratio. To evaluate whether reduced numbers of neutrophil infiltration were directly responsible for the tolerance to oxygen toxicity observed in the Tg mice, we made Wt and Tg mice neutropenic using anti-neutrophil antibodies and subsequently exposed them to 72 hours of hyperoxia. Both Wt and Tg neutrophil-depleted (ND) mice have less severe lung injury compared with non-ND animals, thus providing direct evidence that neutrophils recruited to the lung during hyperoxia play a distinct role in the resultant acute lung injury. We conclude that oxidative and inflammatory processes in the extracellular lung compartment contribute to hyperoxic-induced lung damage and that overexpression of hEC-SOD mediates a protective response to hyperoxia, at least in part, by attenuating the neutrophil inflammatory response.  (+info)

Carbon monoxide provides protection against hyperoxic lung injury. (6/953)

Findings in recent years strongly suggest that the stress-inducible gene heme oxygenase (HO)-1 plays an important role in protection against oxidative stress. Although the mechanism(s) by which this protection occurs is poorly understood, we hypothesized that the gaseous molecule carbon monoxide (CO), a major by-product of heme catalysis by HO-1, may provide protection against oxidative stress. We demonstrate here that animals exposed to a low concentration of CO exhibit a marked tolerance to lethal concentrations of hyperoxia in vivo. This increased survival was associated with highly significant attenuation of hyperoxia-induced lung injury as assessed by the volume of pleural effusion, protein accumulation in the airways, and histological analysis. The lungs were completely devoid of lung airway and parenchymal inflammation, fibrin deposition, and pulmonary edema in rats exposed to hyperoxia in the presence of a low concentration of CO. Furthermore, exogenous CO completely protected against hyperoxia-induced lung injury in rats in which endogenous HO enzyme activity was inhibited with tin protoporphyrin, a selective inhibitor of HO. Rats exposed to CO also exhibited a marked attenuation of hyperoxia-induced neutrophil infiltration into the airways and total lung apoptotic index. Taken together, our data demonstrate, for the first time, that CO can be therapeutic against oxidative stress such as hyperoxia and highlight possible mechanism(s) by which CO may mediate these protective effects.  (+info)

Peripheral chemoreceptor function after carbonic anhydrase inhibition during moderate-intensity exercise. (7/953)

The effect of carbonic anhydrase inhibition with acetazolamide (Acz, 10 mg/kg) on the ventilatory response to an abrupt switch into hyperoxia (end-tidal PO2 = 450 Torr) and hypoxia (end-tidal PO2 = 50 Torr) was examined in five male subjects [30 +/- 3 (SE) yr]. Subjects exercised at a work rate chosen to elicit an O2 uptake equivalent to 80% of the ventilatory threshold. Ventilation (VE) was measured breath by breath. Arterial oxyhemoglobin saturation (%SaO2) was determined by ear oximetry. After the switch into hyperoxia, VE remained unchanged from the steady-state exercise prehyperoxic value (60.6 +/- 6.5 l/min) during Acz. During control studies (Con), VE decreased from the prehyperoxic value (52.4 +/- 5.5 l/min) by approximately 20% (VE nadir = 42.4 +/- 6.3 l/min) within 20 s after the switch into hyperoxia. VE increased during Acz and Con after the switch into hypoxia; the hypoxic ventilatory response was significantly lower after Acz compared with Con [Acz, change (Delta) in VE/DeltaSaO2 = 1.54 +/- 0.10 l. min-1. SaO2-1; Con, DeltaVE/DeltaSaO2 = 2.22 +/- 0.28 l. min-1. SaO2-1]. The peripheral chemoreceptor contribution to the ventilatory drive after acute Acz-induced carbonic anhydrase inhibition is not apparent in the steady state of moderate-intensity exercise. However, Acz administration did not completely attenuate the peripheral chemoreceptor response to hypoxia.  (+info)

Correlation of VEGF expression by leukocytes with the growth and regression of blood vessels in the rat cornea. (8/953)

PURPOSE: To determine the temporal and spatial relationships between neovascularization and basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) mRNA and protein expression in the rat cornea after cautery with silver nitrate. METHODS: In female Sprague-Dawley rats, a silver nitrate applicator was placed on the central cornea to elicit circumferential angiogenesis, and blood vessel growth was quantified by digital image analysis of corneal flat-mounts. Total RNA or protein was extracted from whole corneas until 1 week after cautery, and bFGF and VEGF mRNA and protein levels were determined by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). To localize VEGF mRNA and protein, paraformaldehyde-fixed and paraffin-embedded histologic cross sections of corneas were examined by in situ hybridization and immunohistochemistry. Macrophages were identified by ED2 immunohistochemistry. To examine the regulation of VEGF, rats were treated with dexamethasone (0.5 mg/kg per day) and hyperoxia (70% O2). RESULTS: The neovascular response progresses in three phases: (1) a nonproliferative phase preceding vessel growth (< or = 48 hours after cautery); (2) a proliferative phase with maximal growth rate between 3 and 4 days; and (3) a regressive phase (day 7) with a decrease in vessel density accompanying the completion of vessel elongation. In corneas after cautery, bFGF mRNA expression was unchanged, and bFGF protein concentration decreaseed by 97% after 24 hours and returned to control levels by day 7. In contrast, VEGF164 and VEGF188 mRNA splice variants and protein peaked 48 hours after cautery, remained elevated 4 days after cautery, and decreased to near baseline by day 7. The peak concentration of VEGF in the cornea at 48 hours was calculated to be 720 pM, which is sufficient to evoke a functional response. In situ hybridization and immunohistochemistry showed VEGF expressed initially in neutrophils (24 - 48 hours) and subsequently in macrophages (4 days) adjacent to the cautery site. Treatment with either dexamethasone or systemic hyperoxia inhibited both neovascularization and the increase in VEGF expression. Dexamethasone inhibited 27% of cautery-induced VEGF upregulation at 24 hours and 23% at 48 hours, hyperoxia inhibited 32% at 24 hours and 43% at 48 hours, and combined treatment with both dexamethasone and hyperoxia had an additive effect (56% inhibition at 24 hours). CONCLUSIONS: VEGF production by leukocytes correlates temporally and spatially with cautery-induced angiogenesis in the rat cornea. Both inflammatory products and hypoxia appear to sufficiently increase VEGF expression near the cautery lesion to increase vascular permeability of limbal vessels and induce endothelial cell migration and proliferation.  (+info)

Sevoflurane, a commonly used anesthetic agent has been confirmed to induce cognitive impairment in aged rats. Normobaric hyperoxia preconditioning has been demonstrated to induce neuroprotection in rats. The present study aimed to determine whether normobaric hyperoxia preconditioning could ameliorate cognitive deficit induced by sevoflurane and the possible mechanism by which it may exert its effect. A total of 66, 20‑month‑old male Sprague‑Dawley rats were randomly divided into 3 groups (n=22 each): Rats in the control (C) and sevoflurane anesthesia (S) groups received no normobaric hyperoxia preconditioning before sevoflurane exposure, rats in the normobaric hyperoxia pretreatment (HO) group received normobaric hyperoxia preconditioning before sevoflurane exposure (95% oxygen for 4 continuous h daily for 6 consecutive days). The anesthesia rats (S and HO groups), were exposed to 2.5% sevoflurane for 5 h, while the sham anesthesia rats (C group) were exposed to no sevoflurane. The ...
Bronchopulmonary dysplasia (BPD) is a chronic lung injury characterized by impaired alveologenesis that may persist into adulthood. Rat models of BPD using varying degrees of hyperoxia to produce injury either cause early mortality or spontaneously recover following removal of the inciting stimulus, thus limiting clinical relevance. We sought to refine an established rat model induced by exposure to 60% O from birth by following hyperoxia with intermittent hypoxia (IH). Rats exposed from birth to air or 60% O until day 14 were recovered in air with or without IH (FI = 0.10 for 10 min every 6 h) until day 28 Animals exposed to 60% O and recovered in air had no evidence of abnormal lung morphology on day 28 or at 10-12 wk. In contrast, 60% O-exposed animals recovered in IH had persistently increased mean chord length, more dysmorphic septal crests, and fewer peripheral arteries. Recovery in IH also increased pulmonary vascular resistance, Fulton index, and arterial wall thickness. IH-mediated ...
Atomic force microscopy (AFM), malondialdehyde (MDA) assays, and amperometric measurements of extracellular hydrogen peroxide (H2O2) were used to test the hypothesis that graded hyperoxia induces measurable nanoscopic changes in membrane ultrastructure and membrane lipid peroxidation (MLP) in cultured U87 human glioma cells. U87 cells were exposed to 0.20 atmospheres absolute (ATA) O2, normobaric hyperoxia (0.95 ATA O2) or hyperbaric hyperoxia (HBO2, 3.25 ATA O2) for 60 min. H2O2 (0.2 or 2 mM; 60 min) was used as a positive control for MLP. Cells were fixed with 2% glutaraldehyde immediately after treatment and scanned with AFM in air or fluid. Surface topography revealed ultrastructural changes such as membrane blebbing in cells treated with hyperoxia and H2O2. Average membrane roughness (Ra) of individual cells from each group (n=35 to 45 cells/group) was quantified to assess ultrastructural changes from oxidative stress. The Ra of the plasma membrane was 34±3, 57±3 and 63±5 nm in 0.20 ATA O2, 0.95
Hyperoxia-induced acute lung injury (HALI) is a key contributor to the pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which no specific preventive or therapeutic agent is available. Here we show that lung micro-RNA (miR)-34a levels are significantly increased in lungs of neonatal mice exposed to hyperoxia. Deletion or inhibition of miR-34a improves the pulmonary phenotype and BPD-associated pulmonary arterial hypertension (PAH) in BPD mouse models, which, conversely, is worsened by miR-34a overexpression. Administration of angiopoietin-1, which is one of the downstream targets of miR34a, is able to ameliorate the BPD pulmonary and PAH phenotypes. Using three independent cohorts of human samples, we show that miR-34a expression is increased in type 2 alveolar epithelial cells in neonates with respiratory distress syndrome and BPD. Our data suggest that pharmacologic miR-34a inhibition may be a therapeutic option to prevent or ameliorate HALI/BPD in neonates.
TY - JOUR. T1 - Effect of normobaric hyperoxia on two indexes of synaptic function in fisher 344 rats. AU - Bickford, P. C.. AU - Chadman, K.. AU - Williams, B.. AU - Shukitt-Hale, B.. AU - Holmes, D.. AU - Taglialatela, Giulio. AU - Joseph, J.. PY - 1999/4. Y1 - 1999/4. N2 - The physiological response of two central nervous system neurotransmitter receptors to oxidative stress was studied using the rat model of hyperoxia. We show that hyperoxia leads to a decline in the ability of isoproterenol (ISO) to augment GABAergic responses in cerebellar Purkinje neurons in vivo. This effect is reversed by the N-tert-butyl-α-phenylnitrone (PBN). We also show that hyperoxia produces a decline in the ability of oxotremorine (OXO) to stimulate dopamine (DA) release in striatal slices. This effect is accompanied by an increase in hydroxyl radical levels in the CNS reflected in an increase in 2,3-DHBA, suggesting that the change is the result of an increased level of oxidative stress. We also show a time ...
Fingerprint Dive into the research topics of Angiotensin II type 1 receptor antagonist attenuates lung fibrosis in hyperoxia-exposed newborn rats. Together they form a unique fingerprint. ...
TY - JOUR. T1 - Hyperoxic ventilation exacerbates lung reperfusion injury. AU - Ellman, Peter I.. AU - Alvis, Jeffrey S.. AU - Tache-Leon, Carlos. AU - Singh, Ramesh. AU - Reece, T. Brett. AU - Kern, John A.. AU - Tribble, Curtis G.. AU - Kron, Irving L.. N1 - Funding Information: Supported by the National Institutes of Health under RO1 grant HL506093-03. PY - 2005/11. Y1 - 2005/11. N2 - Objective: It is well known that hyperoxia can be potentially harmful to the ventilated patient, although little is known about the potential effects in the setting of lung reperfusion. We hypothesized that hyperoxic ventilation at the time of reperfusion could worsen the effects of lung reperfusion injury. Methods: Using an ex vivo, blood perfused, isolated rabbit lung system, we evaluated the effects of hyperoxic (fraction of inspired oxygen = 100%, n = 10) versus normoxic (room air, n = 10) ventilation after 18 hours of cold ischemia. Lungs were ventilated and perfused for 2 hours. A control group was ...
TY - JOUR. T1 - Deletion of caveolin-1 protects against oxidative lung injury via up-regulation of heme oxygenase-1. AU - Jin, Yang. AU - Hong, Pyo Kim. AU - Chi, Minli. AU - Ifedigbo, Emeka. AU - Ryter, Stefan W.. AU - Choi, Augustine M.K.. PY - 2008/8/1. Y1 - 2008/8/1. N2 - Acute lung injury (ALI) is a major cause of morbidity and mortality in critically ill patients. Hyperoxia causes lung injury in animals and humans, and is an established model of ALI. Caveolin-1, a major constituent of caveolae, regulates numerous biological processes, including cell death and proliferation. Here we demonstrate that caveolin-1-null mice (cav-1-/-) were resistant to hyperoxia-induced death and lung injury. Cav-1-/- mice sustained reduced lung injury after hyperoxia as determined by protein levels in bronchoalveolar lavage fluid and histologic analysis. Furthermore, cav-1 -/- fibroblasts and endothelial cells and cav-1 knockdown epithelial cells resisted hyperoxia-induced cell death in vitro. Basal and ...
Our main finding is that exposure to hyperoxia was associated with an increased risk for DCI and poor outcome after SAH. As expected, given our selection of high-grade SAH patients, we had a high rate of DCI (38.5%) and poor functional outcome (53.5%). Exposure to hyperoxia was related to approximately three times the risk of DCI and twice the risk of poor 3-months outcome. This relationship was independent of the SAH severity and other comorbidities.. Currently, no guidelines for oxygen therapy in SAH exist. In this study, during the first week after SAH, three quarters of patients were exposed to an average PaO2≥123 mm Hg, and a quarter of patients were exposed to an average PaO2≥173 mm Hg. As seen in our cohort, a recent study has shown that the risk of being exposed to hyperoxia is common in critically ill patients, and such condition was not addressed with any adjustments in ventilator settings.17. Hyperoxia causes oxidative stress by generation of reactive oxygen species and is known ...
We showed that hyperoxia in previously? vitro negatively affects beta cells of the rat. insulin release in mouse neonates. Individuals born preterm displayed higher HbA1c versus controls, as well as insulin resistance. Thus, hyperoxia exerts negative effects in?vitro on human beta cells and results indicate inhibitory effects on insulin secretion in? vivo in mouse neonates. Negative effects might be lessened by the demonstrated speedy and outstanding mitochondrial adaptability. Our results open up the possibility that hyperoxia could affect beta cells of preterm human being neonates negatively. in human being islets (Fig.?3A, overview of B and outcomes, a normal American mark). Pursuing 24?l of hyperoxia structure II was significantly reduced (by 22??4.7%, after earlier hyperoxia, indicated as percentage of corresponding proteins amounts in control islets (normoxia). *after earlier hyperoxia, indicated as percentage of related proteins amounts in control islets (normoxia), *atmospheric air was ...
Hyperoxic acute lung injury (HALI) is characterized by a cell death response with features of apoptosis and necrosis that is inhibited by IL-11 and other interventions. We hypothesized that Bfl-1/A1, an antiapoptotic Bcl-2 protein, is a critical regulator of HALI and a mediator of IL-11-induced cytoprotection. To test this, we characterized the expression of A1 and the oxygen susceptibility of WT and IL-11 Tg(+) mice with normal and null A1 loci. In WT mice, 100% O2 caused TUNEL+ cell death, induction and activation of intrinsic and mitochondrial-death pathways, and alveolar protein leak. Bcl-2 and Bcl-xl were also induced as an apparent protective response. A1 was induced in hyperoxia, and in A1-null mice, the toxic effects of hyperoxia were exaggerated, Bcl-2 and Bcl-xl were not induced, and premature death was seen. In contrast, IL-11 stimulated A1, diminished the toxic effects of hyperoxia, stimulated Bcl-2 and Bcl-xl, and enhanced murine survival in 100% O2. In A1-null mice, IL-11-induced ...
Hyperoxic acute lung injury (HALI) is characterized by a cell death response with features of apoptosis and necrosis that is inhibited by IL-11 and other interventions. We hypothesized that Bfl-1/A1, an antiapoptotic Bcl-2 protein, is a critical regulator of HALI and a mediator of IL-11-induced cytoprotection. To test this, we characterized the expression of A1 and the oxygen susceptibility of WT and IL-11 Tg(+) mice with normal and null A1 loci. In WT mice, 100% O2 caused TUNEL+ cell death, induction and activation of intrinsic and mitochondrial-death pathways, and alveolar protein leak. Bcl-2 and Bcl-xl were also induced as an apparent protective response. A1 was induced in hyperoxia, and in A1-null mice, the toxic effects of hyperoxia were exaggerated, Bcl-2 and Bcl-xl were not induced, and premature death was seen. In contrast, IL-11 stimulated A1, diminished the toxic effects of hyperoxia, stimulated Bcl-2 and Bcl-xl, and enhanced murine survival in 100% O2. In A1-null mice, IL-11-induced ...
Hyperoxic acute lung injury (HALI) is characterized by a cell death response with features of apoptosis and necrosis that is inhibited by IL-11 and other interventions. We hypothesized that Bfl-1/A1, an antiapoptotic Bcl-2 protein, is a critical regulator of HALI and a mediator of IL-11-induced cytoprotection. To test this, we characterized the expression of A1 and the oxygen susceptibility of WT and IL-11 Tg(+) mice with normal and null A1 loci. In WT mice, 100% O2 caused TUNEL+ cell death, induction and activation of intrinsic and mitochondrial-death pathways, and alveolar protein leak. Bcl-2 and Bcl-xl were also induced as an apparent protective response. A1 was induced in hyperoxia, and in A1-null mice, the toxic effects of hyperoxia were exaggerated, Bcl-2 and Bcl-xl were not induced, and premature death was seen. In contrast, IL-11 stimulated A1, diminished the toxic effects of hyperoxia, stimulated Bcl-2 and Bcl-xl, and enhanced murine survival in 100% O2. In A1-null mice, IL-11-induced ...
Thesis Advisor Alan Wells, MD, DMS. Research Project Information. I am investigating whether metastatic breast carcinoma cells require E-cadherin re-expression to integrate and to confer a survival advantage in the liver, a common site of breast cancer metastases. Publications Yeh JJ, Munson K, Chao Y, Peterson QP, MacRae CA, Peterson RT (2007). AML1-ETO Reprograms Hematopoietic Cell Fate in Zebrafish. Submitted.. De Paepe ME, Mao Q, Chao Y, Powell JL, Rubin LP, Sharma S. (2005). Hyperoxia-induced apoptosis and Fas/FasL expression in lung epithelial cells. Am J Physiol Lung Cell Mol Physiol. Oct;289(4):L647-59.. Zhou HW, Nussbaumer C, Chao Y, DeLong A. (2004). Disparate roles for the regulatory A subunit isoforms in Arabidopsis. Plant Cell. Mar;16(3):709-2 Abstracts:. DePaepe ME, Chao Y, Mao QF. (2004). Hyperoxia-induced apoptosis and apoptotic gene expression in lung epithelial cells. Developmental Biology of the Lung, Montreal, Canada, May. Presentations:. Chao Y, Shepard CR, Wells, A. ...
16. Frank L. Developmental aspects of experimental pulmonary oxygen toxicity. Free Radic Biol Med. 1991;11(5):463-94. PMID: 1769607. 17. Frank L, Bucher JR, Roberts RJ. Oxygen toxicity in neonatal and adult animals of various species. J Appl Physiol Respir Environ Exerc Physiol. 1978;45(5):699-704. PMID: 730565. 18. Clark JM, Lambertsen CJ. Pulmonary oxygen toxicity: a review. Pharmacol Rev. 1971;23(2):37-133. PMID: 4948324. 19. Robinson FR, Casey HW, Weibel ER. Animal model: oxygen toxicity in nonhuman primates. 2010;15(4):230-5. 007. Epub 2010 May 10. PMID: 20452844. 5. Velten M, Heyob KM, Rogers LK, Welty SE. Deficits in lung alveolarization and function after systemic maternal inflammation and neonatal hyperoxia exposure. J Appl Physiol (1985). 2010;108(5):1347-56. 2009. Epub 2010 Mar 11. PMID: 20223995. 6. Deulofeut R, Critz A, Adams-Chapman I, Sola A. Avoiding hyperoxia in infants < or = 1250 g is associated with improved short- and long-term outcomes. J Perinatol. 2006;26(11):700- 5. Epub ...
TY - JOUR. T1 - Cathelicidin attenuates hyperoxia-induced intestinal injury through inhibition of NF-κB activity in newborn rats. AU - Chou, Hsiu Chu. AU - Chen, Chung Ming. PY - 2019/1/1. Y1 - 2019/1/1. N2 - Supplemental oxygen is often used to treat neonates with respiratory disorders. Preclinical studies have demonstrated that neonatal hyperoxia injures the distal small intestine and activates nuclear factor-κB (NF-κB). Cathelicidin inhibits NF-κB activity and ameliorates lipopolysaccharide-induced intestinal barrier disruption in rats. Sprague-Dawley rat pups were reared in either room air (RA) or hyperoxia (85% O2) and were randomly treated with low-dose cathelicidin (4 mg/kg, LDC) and high-dose cathelicidin (HDC, 8 mg/kg) in 0.05 mL of normal saline (NS) administered intraperitoneally on postnatal days 1-6. The following six groups were obtained: RA + NS, RA + LDC, RA + HDC, O2 + NS, O2 + LDC, and O2 + HDC. The animals were sacrificed and the terminal ileum was removed for Western blot ...
This study combines two well-known vascular research models, hyperoxia and hind limb ischemia, aiming to better characterize capacities of the hyperoxia challenge. We studied two groups of C57/BL6 male mice, a control (C) and a hind limb ischemia (HLI) group. Perfusion from both limbs was recorded in all animals by laser Doppler techniques under an oxygen (O 2) saturated atmosphere, once for control and, during 35 days for the HLI group. We used a third set of normoxic animals for HLI morphometric control. The expected variability of responses was higher for the younger animals. In the HLI group, capillary density normalized at Day 21 as expected, but not microcirculatory physiology. In the operated limb, perfusion decreased dramatically following surgery (Day 4), as a slight reduction in the non-operated limb was also noted. Consistently, the response to hyperoxia was an increased perfusion in the ischemic limb and decreased perfusion in the contralateral limb. Only at Day 35, both limbs exhibited
Several previous studies have shown that when the partial pressure of oxygen in the blood increases, blood flow decreases, presumably as the result of localised vasoconstriction.13,14,30-33 This finding was confirmed for the normal group, in whom a reduction in both the PSV and EDV was apparent in the OA in response to hyperoxia. As described earlier, the finding of reduced PSV and EDV in tandem is considered to be indicative of reduced volumetric flow.29 Conversely, no significant change in blood flow was observed for the glaucoma group. The absence of any response in the glaucoma group would seem to support the hypothesis of pre-existing vasospasm, creating an inability to constrict further under hyperoxic conditions.. The finding that blood flow measures reduced in the OA but not CRA or SPCAs of the normal group only could be attributed to the reduction in IOP seen in this group. As IOP decreases OPP increases thus increasing blood flow.34 The smaller calibre vessels of the ocular ...
OBJECTIVE: The relative contributions of the fraction of inspired oxygen (FIO2) and atmospheric pressure (ATM) to cardioprotection are unknown. We determined whether the product of FIO2 x ATM (oxygen partial pressure) controls the extent of hyperoxic+hyperbaric-induced cardioprotection and involves activation of nitric oxide synthase (NOS).. METHODS: Adult Sprague Dawley rats (n = 10/gp) were treated for 1 h with (1) normoxia+normobaria (21% O2 at 1 ATM), (2) hyperoxia+normobaria (100% O2 at 1 ATM), (3) normoxia+hyperbaria (21% O2 at 2 ATM) and (4) hyperoxia+hyperbaria (100% O2 at 2 ATM).. RESULTS: Infarct size following 25 min ischemia and 180 min reperfusion was decreased following hyperoxia+normobaria and normoxia+hyperbaria compared with normoxia+normobaria and further decreased following hyperoxia+hyperbaria treatment. l-NAME (200 microM) reversed the cardioprotective effects of hyperoxia+hyperbaria. Nitrite plus nitrate content was increased 2.2-fold in rats treated with ...
Results Of the 680 patients presenting with AECOPD in the review period, 254 presentations in 180 patients had data suitable for analysis. Hyperoxaemia occurred in 61/254 (24%) presentations and was strongly associated with serious adverse outcome compared with normoxaemia (OR 9.17, 95% CI 4.08 to 20.6). Hypoxaemia was also associated with an increased risk of serious adverse outcome compared with normoxaemia (OR 2.16, 95% CI 1.11 to 4.20). Compared with the recommended target oxygen saturation range of 88%-92%, the risk of a serious adverse outcome was increased in both the ,88% group (OR 2.0, 95% CI 1.03 to 3.80) and the ,96% group (OR 2.37, 95% CI 1.34 to 4.20).. ...
Irradiation with light wavelengths from the far red (FR) to the near infrared (NIR) spectrum (600 nm -1000 nm) has been shown to have beneficial effects in several disease models. In this study, we aim to examine whether 670 nm red light pretreatment can provide protection against hyperoxia-induced damage in the C57BL/6J mouse retina. Adult mice (90-110 days) were pretreated with 9 J/cm2 of 670 nm light once daily for 5 consecutive days prior to being placed in hyperoxic environment (75% oxygen). Control groups were exposed to hyperoxia, but received no 670 nm light pretreatment. Retinas were collected after 0, 3, 7, 10 or 14 days of hyperoxia exposure (n = 12/group) and prepared either for histological analysis, or RNA extraction and quantitative polymerase chain reaction (qPCR). Photoreceptor damage and loss were quantified by counting photoreceptors undergoing cell death and measuring photoreceptor layer thickness. Localization of acrolein, and cytochrome c oxidase subunit Va (Cox Va) were identified
Resveratrol could protect lungs from hyperoxia-induced injury through its antioxidant, anti-inflammatroy and anti-fibrotic effects.
Sigma-Aldrich offers abstracts and full-text articles by [Hongping Xia, Xiaomeng Ren, Craig S Bolte, Vladimir Ustiyan, Yufang Zhang, Tushar A Shah, Tanya V Kalin, Jeffrey A Whitsett, Vladimir V Kalinichenko].
Inhaled nitric oxide is potentially beneficial in preterm infants for two main reasons. First, it may improve gas exchange in infants with established respiratory failure through enhanced ventilation-perfusion matching and/or a reversal of extrapulmonary shunting resulting in a lowering of respiratory support requirements and hence reduced ventilator and oxygen-induced lung injury.4 Second, inhaled nitric oxide has been shown to reduce lung inflammation and oxidant stress, preserve surfactant function, and promote lung growth and pulmonary vascular development in various laboratory studies and experimental models of bronchopulmonary dysplasia (BPD).5-10 These effects of inhaled nitric oxide may potentially attenuate preterm lung injury and therefore reduce the risk or severity of BPD if it is used at an early stage in the disease process. ...
Clinical Trials - clinicaltrials.gov Several studies show how patients with hyperoxia after cardiac arrest has increased mortality, but the association of hyper...
Ventilation of preterm babies with infant respiratory distress syndrome (IRDS) using high oxygen pressures is often a life-saving therapy. A severe side effect of this therapeutic hyperoxia though, is the formation of reactive oxygen species that are involved in the pathogenesis of different lung diseases. This thesis is designed to develop models for oxidative stress in the lung and to further characterise the mechanisms of oxidative damage. The following models have been examined: 1. Examination of isolated type II cells from hyperoxia-exposed and control rats (in vivo). 2. Cultivation of isolated type II cells in the presence of H2O2 (in vitro). In this thesis we show that only by cultivating type II cells under basal conditions the expression of heat shock proteins (HSP) is strongly activated, whereas freshly isolated cells do not express HSP. We conclude in accordance with the newer literature, that the basal cell culture conditions alone can represent a stress factor for the cells. Under ...
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Looks like divers arent the only ones who need to be aware of hyperoxia: NASA Decodes Trouble With F-22 Issue has actually been a poorly understood concern within the Raptor community for a while now.
Maturational differences in lung NF-κB activation and their role in tolerance to hyperoxia: Neonatal rodents are more tolerant to hyperoxia than adults. We dete
We quantified the effects of continuous exposure to 100% 02 on the development of sublethal injury to the pulmonary alveolar epithelium of rabbits. There was a progressive increase in alveolar permeability to solute after 48 h in 0 which coincided with the onset of damage to the pulmonary microvasculature. Rabbits that were exposed to 100% O2for 64 h and returned to room air for 24 h had, in addition to increased permeability to solute, decreased phospholipid levels, decreased total lung capacity, pulmonary edema, high minimum surface tensions in their bronchoalveolar lavage, and moderate hypoxemia. Intratracheal instillation of calf lung surfactant (CLSE) significantly ameliorated the progression of hyperoxic injury by increasing alveolar phospholipid levels and thus preventing the inhibition of lung surfactant activity by plasma proteins and other high molecular weight components of alveolar edema. We concluded that the alveolar epithelium and the pulmonary microvasculature show similar ...
The results presented in this study show that inflammasome formation and IL-1β processing is induced by hyperoxia in vivo and in vitro and is associated with increased alveolar epithelial protein permeability. Hyperoxia-stimulated K+ efflux, inflammasome formation, proinflammatory cytokine release, and marked induction of caspase-1 and IL-1β cleavage. The P2X7 agonist ATP enhanced hyperoxia-induced inflammasome activation, whereas the P2X7 antagonist, oxATP, inhibited hyperoxia-induced inflammasome activation. However, when ATP was scavenged with apyrase, hyperoxia-induced inflammasome activation was significantly decreased, indicating the possible involvement of the P2X7 receptor. Furthermore, shRNA silencing of inflammasome component expression abrogated hyperoxia-induced secretion of proinflammatory cytokines in vitro. These results suggest that hyperoxia induces K+ efflux through the P2X7 receptor and leads to inflammasome activation and secretion of proinflammatory cytokines.. Our studies ...
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TY - JOUR. T1 - The use of hyperoxia to induce chronic mild oxidative stress in RPE cell in vitro. AU - Honda, Shigeru. AU - Hjelmeland, Leonard M. AU - Handa, James T.. PY - 2001. Y1 - 2001. N2 - Purpose: To establish a model of mild and chronic oxidative stress using hyperoxia for retinal pigment epithelial (RPE) cells in vitro. Methods: RPE340 cells and WI38 lung fibroblasts were grown in normal oxygen (20% O2) and hyperoxia (40% O2 or 60% O2). After cell viability was examined, the levels of reactive oxygen intermediates (ROI) by flow cytometry and heme oxygenase-1 (HO-1) mRNA by northern analysis were measured as markers of oxidative stress in both cell types. Proliferative ability and gene expression pattern of growth factors were studied to demonstrate the phenotypic changes induced by mild oxidative stress upon these cells. Results: While decreased by 60% O2, 40% O2 did not affect viability in both cell types, ROI production and HO-1 mRNA expression were elevated in hyperoxia compared to ...
Arterial spin labelling allows simultaneous measurement of both the blood-oxygenation-level-dependent (BOLD) and the cerebral blood flow (CBF) response to changes in neural activity. The addition of a hypercapnia or hyperoxia calibration allows additional quantification of changes in the cerebral metabolic rate of oxygen (CMRO(2)). In this study we test the reproducibility of measurements derived using the hyperoxia approach, during a cognitive Stroop task. A QUIPSSII sequence is used at 3 T to collect simultaneous CBF and BOLD signal during two 3 min periods of hyperoxia and an 8 min Stroop task. Hyperoxia was administered via an open system and end-tidal values were sampled via a nasal cannula; average end-tidal values of 60% were reached. This procedure is repeated to allow the reproducibility of the estimated parameters to be tested. The use of a cognitive Stroop task allows testing of the measurements in frontal and parietal regions as well as sensorimotor areas in which previous studies have been
Background. Hypoxia resultant from haemorrhagic shock is the primary cause of kidney damage. Application of normobaric hyperoxia therapy (NHT) is an acceptable treatment for acute haemorrhagic shock. We investigated the effect of NHT on amelioration of haemorrhagic shock-induced rat renal failure.. Methods. Twenty-four Sprague-Dawley rats were subjected to gradual blood withdrawal/reperfusion, followed by 12-h, 24-h or 48-h NHT. Verification/monitoring of intrarenal hypoxia was performed using Hypoxyprobe-TM-1. Subsequently, cystatin C, urea and creatinine were assessed in serum by a Hitachi autoanalyser, and NO, 3-nitro-tyrosine, STAT-8-isoprostane and NF-kB in renal medullae and cortices by specific ELISAs.. Results. In rats subjected to haemorrhagic shock, 12- to 48-h NHT significantly reduced intrarenal Hypoxyprobe-TM-1 stained areas and attenuated augmentation of urea, creatinine and cystatin C. Haemorrhagic shock resulted in a 10-fold drop of intrarenal NO availability. 12-h and 24-h, but ...
Przyklenk, A, Aussieker, T, Gutmann, B, Schiffer, T, Brinkmann, C, Strüder, HK, Bloch, W, Mierau, A, and Gehlert, S. Effects of endurance exercise bouts in hypoxia, hyperoxia, and normoxia on mTOR-related protein signaling in human skeletal muscle. J Strength Cond Res XX(X): 000-000, 2018-This study investigated the effects of short-term hypoxia (HY), hyperoxia (PER), and normoxia on anabolic signaling proteins in response to an acute bout of moderate endurance exercise (EEX) before and after an endurance exercise training intervention. Eleven healthy male subjects conducted one-legged cycling endurance exercise (3 × 30 min·wk for 4 weeks). One leg was trained under hypoxic (12% O2) or hyperoxic conditions (in a randomized cross-over design), and the other leg was trained in normoxia (20.9% O2) at the same relative workload. Musculus vastus lateralis biopsies were taken at baseline (T0) as well as immediately after the first (T1) and last (T2) training session to analyze anabolic signaling ...
This study investigated the effects of hyperoxic treatment on growth, angiogenesis, apoptosis, general morphology and gene expression in DMBA-induced rat mammary tumors. One group of animals was exposed to normobaric hyperoxia (1 bar, pO2 = 1.0 bar) and another group was exposed to hyperbaric hyperoxia (1.5 bar, pO2 = 1.5 bar). A third group was treated with the commonly used chemotherapeutic drug 5- Fluorouracil (5-FU), whereas animals housed under normal atmosphere (1 bar, pO2 = 0.2 bar) served as controls. All treatments were performed on day 1, 4, 7 and 10 for 90 min. Tumor growth was calculated from caliper measurements. Biological effects of the treatment, was determined by assessment of vascular morphology (immunostaining for von Willebrandt factor) and apoptosis (TUNEL staining). Detailed gene expression profiles were obtained and verified by quantitative rtPCR. Tumor growth was significantly reduced (~57-66 %) after hyperoxic treatment compared to control and even more than 5-FU (~36 %). Light
Bronchopulmonary dysplasia is a chronic lung disease of premature neonates characterized by arrested pulmonary alveolar development. There is increasing evidence that microRNAs (miRNAs) regulate translation of messenger RNAs (mRNAs) during lung organogenesis. The potential role of miRNAs in the pathogenesis of BPD is unclear. Following exposure of neonatal mice to 80% O2 or room air (RA) for either 14 or 29 days, lungs of hyperoxic mice displayed histological changes consistent with BPD. Comprehensive miRNA and mRNA profiling was performed using lung tissue from both O2 and RA treated mice, identifying a number of dynamically regulated miRNAs and associated mRNA target genes. Gene ontology enrichment and pathway analysis revealed that hyperoxia modulated genes involved in a variety of lung developmental processes, including cell cycle, cell adhesion, mobility and taxis, inflammation, and angiogenesis. MiR-29 was prominently increased in the lungs of hyperoxic mice, and several predicted mRNA targets of
TY - JOUR. T1 - The effect of leptin on the ventilatory response to hyperoxia. AU - Groeben, Harald. AU - Meier, Sascha. AU - Brown, Robert H.. AU - ODonnell, Christopher P.. AU - Mitzner, Wayne. AU - Tankersley, Clarke G.. PY - 2004/10/1. Y1 - 2004/10/1. N2 - Leptin-deficient mice show a blunted response to hypercapnia explained by central nervous system effects. The impact of leptin on peripheral chemoreceptor function is unclear. Therefore, 9 mutant (ob/ob) and 9 wild-type (+/+) mice were exposed to room air or 100% oxygen and respiratory rate (RR) and tidal volume (Vt) were measured. Subsequently, ob/ob mice received either leptin or vehicle and measurements were repeated. Compared to baseline, for +/+ mice, RR decreased significantly by 9.4% ± 3.0% (means ± SD), whereas Vt remained unchanged. Transition from normoxia to hyperoxia did not change RR and Vt in untreated ob/ob mice, whereas after leptin treatment, RR and Vt decreased significantly. Leptin deficiency abolishes the response to ...
Project 1. Ozone (O3) is a major component of air pollution and it has important detrimental health effects on humans. Moreover, as much as 40% of the U.S. population is estimated to be exposed to potentially harmful levels of O3. We previously identified significant linkage of O3-induced lung hyperpermeability and inflammation QTLs to chromosomes 4 and 17 (Inf2), respectively. Ongoing research in the EGG has addressed the hypotheses that gene(s) within the chromosome 4 QTL [e.g. toll-like receptor 4 (Tlr4)] and Inf2 [e.g. tumor necrosis factor alpha (Tnf)] modulate differential susceptibility to O3-induced injury and inflammation.. Project 2. Reactive oxygen species (ROS) have been implicated in the pathogenesis of many acute and chronic clinical disorders such as acute lung injury, bronchopulmonary dysplasia (BPD), and cancer. The transcription factor NF-E2, related factor 2 (Nrf2) was identified as a candidate susceptibility gene for hyperoxia-induced lung injury and inflammation in adult ...
Treatment of rat pups with hyperoxia-induced lung injury, an in vivo model for experimental BPD (41), with metformin prolongs survival; reduces lung injury by attenuating lung inflammation, coagulation, septal thickness, and collagen III expression; and stimulates vascularization. Metformin had no beneficial effects on alveolarization, capillary alveolar leakage, arterial medial wall thickness (PAH), and RVH, and no adverse effects on normal lung and heart development. These data demonstrate that metformin may be a suitable candidate to reduce lung inflammation, coagulation, and fibrosis in preterm infants with severe BPD.. Metformin is a potent antidiabetic drug that is commonly used in type 2 diabetic patients to lower glucose levels in the circulation. Compared with other treatment modalities for type 2 diabetes, patients treated with metformin were protected against mortality in cardiac disease and had less cancer, suggesting that metformin has various biological functions other than its ...
Aim: Effective treatment of premature infants with bronchopulmonary dysplasia (BPD) is lacking. We hypothesize that bone morphogenetic protein 9 (BMP9), a ligand of the TGF-β family that binds to the activin receptor-like kinase 1 (ALK1)-BMP receptor type 2 (BMPR2) receptor complex, may be a novel therapeutic option for BPD. Therefore, we investigated the cardiopulmonary effects of BMP9 in neonatal Wistar rats with hyperoxia-induced BPD. Methods: Directly after birth Wistar rat pups were exposed to 100% oxygen for 10 days. From day 2 rat pups received BMP9 (2.5 µg/kg, twice a day) or 0.9% NaCl by subcutaneous injection. Beneficial effects of BMP9 on aberrant alveolar development, lung inflammation and fibrosis, and right ventricular hypertrophy (RVH) were investigated by morphometric analysis and cytokine production. In addition, differential mRNA expression of BMP9 and its receptor complex: ALK1, BMPR2 and Endoglin, and of the ALK1 downstream target transmembrane protein 100 (TMEM100) were studied
Having confirmed the ability of myr-Akt to induce activation of downstream signaling pathways in lung epithelial cells, we investigated whether expression of Ad-myr-Akt could prevent oxidant-induced lung injury and death in animals. In these experiments, control adenovirus or adenovirus expressing myr-Akt 17 was introduced intratracheally into mice and the mice were immediately exposed to 100% O2. Although all of the control mice died within 72 h of initiation of exposure to 100% O2, all of the mice infected with Ad-myr-Akt lived longer (Fig. 2). The mice were killed at 120 h at which point they had begun to display respiratory distress. Thus, mice expressing activated Akt showed a significant increase in survival time (P , 0.0001). Histological examination of lung sections showed hyaline membrane formation, hemorrhage, inflammation, and gross pulmonary edema in the lungs of the control mice at 72 h (Fig. 3 A). In contrast, the lungs of mice infected with Ad-myr-Akt appeared normal and free of ...
Adult hamsters were exposed to 100% oxygen for up to 8 days. At time of death lung tissue was analyzed for the expression of surfactant protein (SP) genes, and surfactant was isolated from alveolar lavage fluid. Surfactant was analyzed for the composition of proteins and phospholipids and for its surface properties. We found, over the 8 days of exposure, that an alveolitis composed of polymorphonuclear leukocytes (PMNs) and alveolar macrophages, accompanied by exudation of edema fluid, appeared in the alveolar spaces. The steady-state levels of SP mRNAs declined after 8 days of exposure to 100% oxygen, but the patterns indicated individual genetic control. SP-A was elevated early in the course of the hyperoxic exposure but decreased significantly by day 8; SP-B decreased continuously; SP-C was unchanged (or slightly elevated) through day 2 and then declined. The amounts of recoverable lavage surfactant increased by greater than threefold, and the phospholipid composition showed increasing percentages of
In the present RCT in patients undergoing scheduled isolated CABG surgery, we found no difference in markers of myocardial damage between a conventional moderate hyperoxic and a near-physiological oxygen strategy during and after surgery. The conservative oxygenation strategy did not improve haemodynamics in comparison to moderate hyperoxia. However, lower oxygen targets during CPB and ICU admission could be applied safely without risk of hypoxia.. With respect to myocardial damage, these findings are in apparent contrast to results from earlier clinical trials where the reduction of oxygen tension during CPB or reperfusion resulted in lower CK (672 ± 130 vs. 293 ± 21 U/l; P = 0.002) [1] or lower Troponin-T levels (~2.1 vs. ~0.8 μg/L; P , 0.05) [2]. However, the high PaO2 investigated in the latter two studies are no longer applied today. The first study compared a PaO2 of ~400 mmHg during CPB in the control group to ~140 mmHg in the conservative group [2]. The second study compared ...
In a study of 6 men aged 29 to 48 we studied the effect of water body immersion during air or pure oxygen, or oxygen - 4 % CO2 gas mixture breathing upon pulmonary volumes and respiratory biomechanics (using bodyplethysmography), the extent of lung hydration (two-frequency impedansometry), and pulmonary metabolic function (by determination of the concentration of biologically active substances in the condensate of the exhaled air). We found an additive nature of immersion/hyperoxic effects upon the respiratory and metabolic pulmonary functions manifested in an acceleration and growth of a deficit in pulmonary vital capacity, a bronchoconstriction effect, increase of a lung hydration, and decrease of serotonin catabolism. Contrary to our expectation, we did non find any potentiation of oxygen induced toxic effects upon the lungs during immersion/hyperoxia/hypercapnia exposures ...
The time to onset of symptoms is highly variable but most individuals can tolerate 12-16 hours of oxygen at 1.0 ATA, 8-14 hours at 1.5 ATA, and 3-6 hours at 2.0 ATA before developing mild symptoms. There are several ways to track developing pulmonary oxygen toxicity but the most sensitive and accurate is the development of symptoms. A second technique is to monitor the vital capacity. Vital capacity (the amount of air that can be moved in one large breath) decreases with increasing pulmonary toxicity. A reduction of approximately 2% in vital capacity correlates with mild symptoms while a reduction of 10% correlates symptoms so severe that most individuals will not voluntarily continue breathing oxygen. These mild effects are completely reversible and no permanent lung damage occurs. However, the damage will take 2 to 4 weeks to heal. The pathology of pulmonary oxygen toxicity is understood but beyond the scope of this discussion.. A third way to keep track, in rough terms, of pulmonary oxygen ...
There is animal evidence that inhaled nitric oxide (NO) reduces lung inflammation, improves surfactant function, attenuates hyperoxic lung injury, and promotes lung growth. It is hoped, therefore, that it might prevent bronchopulmonary dysplasia (BPD). Trials in preterm infants with respiratory failure have, however, given inconclusive results. Now two US multicentre trials have provided some support for treatment with inhaled NO.. In a 21-centre trial ...
The authors report changes in the way the lung grows from early exposure to ozone. The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology http://onlinelibrary.wiley.com/doi/10.1002/ar.22545/abstract Ozone Exposure During the Early Postnatal Period Alters the Timing and Pattern of Alveolar Growth and Development in Nonhuman Primates Abstract Exposure to oxidant air pollutants in early childhood,…
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Following renal ischemia-reperfusion injury (RIRI), because of the decrease in oxygen supply to the kidney, a large amount of oxygen-free radicals is generated, and in severe cases, tissue cells will undergo apoptosis or even die. Normobaric hyperoxia (NBHO) is a very common clinical adjuvant treatment. It restores the oxygen supply after renal ischemia and combats oxidative stress in tissues, thus playing a protective role. In this study, our aim is to elucidate the protective mechanism of NBHO inhalation in a rat RIRI model. We performed a surgical excision of the left kidney of the rat and established a right kidney solitary kidney model. Later, the right renal pedicle of the rat was clamped using a non-invasive vascular clamp for 45 min. After the vascular clamp was released and reperfused for 24 h, the rat was placed in a closed oxygen chamber. It was subjected to inhalation of high-concentration oxygen (50%-55%), 2 h daily, for 7 days.RIRI induces postoperative weight loss, impaired renal ...
It is the policy of the University of Wisconsin-Madison ICEP that the faculty, authors, planners, and other persons who may influence content of this CE activity disclose all relevant financial relationships with commercial interests* in order to allow CE staff to identify and resolve any potential conflicts of interest. Faculty must also disclose any planned discussions of unlabeled/unapproved uses of drugs or devices during the educational activity. For this educational activity all conflicts of interests have been resolved and detailed disclosures are listed below:. Mark Robitaille, MD: No relevant relationships to disclose in regard to this activity ...
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Narimanbekov I.O.; Rozycki H.J., 1992: Hyperoxic hyperventilation induced lung damage manifested within eight hours in a rabbit model
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Excess Oxygen can cause pulmonary oxygen toxicity which results in a lot of damage to the body tissues. To summarize briefly, the excess oxygen can cause..
Children born with heart defects that pummel their lungs with up to three times the normal blood volume quickly find their lungs in jeopardy as well.
Retinal, Association, Blood, Blood Vessels, Human, Hyperoxia, Light, Microvasculature, Retinal Blood Vessels, Vasoconstriction, Vasodilation
Must work to reduce the risk of post-ROSC hyperoxia. In general, dial down FiO2 to 60% as soon as tolerated by pt. (keep pt sat around 94%, no need to get to 100%, may be harmful ...
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Eduardo Bancalari, MD has won several academic and professional awards within the pediatrics and neonatology fields and is an author of The Newborn Lung.
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... is the opposite of hypoxia; hyperoxia refers to a state in which oxygen supply is excessive, and hypoxia refers to a ... Hyperoxia occurs when cells, tissues and organs are exposed to an excess supply of oxygen (O2) or higher than normal partial ... This kind of hyperoxia can lead to oxygen toxicity, caused from the harmful effects of breathing molecular oxygen at elevated ... Breathing nitrox can lead to hyperoxia due to the high partial pressure of oxygen if used too deep or for too long. Protocols ...
A hyperoxia test is a test that is performed-usually on an infant-to determine whether the patient's cyanosis is due to lung ...
Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in ... Hyperoxia can also indirectly cause carbon dioxide narcosis in patients with lung ailments such as chronic obstructive ... The result of breathing increased partial pressures of oxygen is hyperoxia, an excess of oxygen in body tissues. The body is ... Protocols for avoidance of the effects of hyperoxia exist in fields where oxygen is breathed at higher-than-normal partial ...
Jamieson, D; Chance, B; Cadenas, E; Boveris, A (1986). "The relation of free radical production to hyperoxia". Annual Review of ...
Dise CA, Clark JM, Lambertsen CJ, Goodman DB (February 1987). "Hyperbaric hyperoxia reversibly inhibits erythrocyte ... "Hypoxic ventilatory sensitivity in men is not reduced by prolonged hyperoxia (Predictive Studies V and VI)". J. Appl. Physiol. ... "Ventilatory effects of prolonged hyperoxia at pressures of 1.5-3.0 ATA". Aviat Space Environ Med. 77 (8): 801-10. PMID 16909873 ... "Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA". J. Appl. Physiol. 95 ...
Pulse oximetry can guide the use of supplemental oxygen to maintain oxygen saturation greater than 94%. Hyperoxia should be ...
Sheng M, Liu P, Mao D, Ge Y, Lu H (2017-05-02). "The impact of hyperoxia on brain activity: A resting-state and task-evoked ... Hyperoxia at normobaric environments does not appear to be able to halt erythropoiesis completely. Within the lungs, hypoxia is ... Hyperoxia is observed to result in a serum reduction in erythropoietin, resulting in reduced stimulus for erythropoiesis. ... Cases in which an excess amount of oxygen is available to organs is known as hyperoxia. While the following effects may ...
There are adverse effects involved with rat placement in hyperoxia condition. Hypercapnia is a condition where there is high ...
MacLaughlin KJ, Barton GP, Braun RK, Eldridge MW (July 2019). "Effect of intermittent hyperoxia on stem cell mobilization and ...
"Recombinant Plasma Gelsolin Diminishes the Acute Inflammatory Response to Hyperoxia in Mice". Journal of Investigative Medicine ...
"Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia". J. Exp. Biol. 204 (Pt 18 ...
von Zglinicki, T., Saretzki, G., Docke, W., and Lotze, C. (1995). Mild hyperoxia shortens telomeres and inhibits proliferation ...
Singhal AB, Wang X, Sumii T, Mori T, Lo EH (July 2002). "Effects of normobaric hyperoxia in a rat model of focal cerebral ... Shin HK, Dunn AK, Jones PB, Boas DA, Lo EH, Moskowitz MA, Ayata C (June 2007). "Normobaric hyperoxia improves cerebral blood ... at ClinicalTrials.gov Henninger N, Bouley J, Nelligan JM, Sicard KM, Fisher M (September 2007). "Normobaric hyperoxia delays ...
The physiologic consequences contain hypoxia, sleep fragmentation, autonomic nervous system dysregulation or hyperoxia. The ...
"Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia". The Journal of ...
Ramesh Babu, Polani B.; Chidekel, Aaron; Shaffer, Thomas H. (Mar 2005). "Hyperoxia-induced changes in human airway epithelial ...
"Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia". The Journal of ...
Preterm infants can be monitored reducing cerebral hypoxia and hyperoxia with different patterns of activities. It is an ...
... sensitive to hyperoxia). In plants, SOD isozymes are present in the cytosol and mitochondria, with an iron SOD found in ... "Mice deficient in cellular glutathione peroxidase develop normally and show no increased sensitivity to hyperoxia". The Journal ...
"Collagen and elastin cross-linking is altered during aberrant late lung development associated with hyperoxia". American ...
... also contributes to tissue injury following irradiation and hyperoxia, as well as in diabetes. In ...
Normobaric hyperoxia protects against demyelination in an experimental model of pattern III multiple sclerosis lesions. In: ( ...
Hyperoxia in the late Paleozoic atmosphere may have physiologically enhanced the initial evolution of tetrapod locomotor ... Experimentally, the biomechanical and physiological effects of hyperoxia on animal flight performance can be decoupled through ...
... an effort to reduce hyperoxia in the neonatal intensive care unit". J Perinatol. 34 (1): 33-8. doi:10.1038/jp.2013.122. PMID ... and may enable proactive interventions to avoid hypoxia and unintended hyperoxia.[citation needed] Patient SafetyNet is a ...
Hyperoxia in the late Paleozoic atmosphere may have physiologically enhanced the initial evolution of tetrapod locomotor ... Experimentally, the biomechanical and physiological effects of hyperoxia on animal flight performance can be decoupled through ...
Too high a concentration of oxygen results in hyperoxia, leading to oxygen toxicity, a condition causing convulsions which can ... The consequences can include hypoxia, hyperoxia, and incorrect decompression information, all three of which are potentially ...
The result of breathing increased partial pressures of oxygen is hyperoxia, an excess of oxygen in body tissues. The body is ... Protocols for avoidance of the effects of hyperoxia exist in fields where oxygen is breathed at higher-than-normal partial ...
Modified oxygen mask to induce target levels of hyperoxia and hypercarbia during radiotherapy: a more effective alternative to ...
Sicard KM, Duong TQ (April 2005). "Effects of hypoxia, hyperoxia, and hypercapnia on baseline and stimulus-evoked BOLD, CBF, ...
Millicovsky G, Johnston MC (Sep 1981). "Hyperoxia and hypoxia in pregnancy: simple experimental manipulation alters the ...
An additional mechanism proposes seizure onset as a result of hyperoxia induced enzyme inhibition, notably of Gama Amino ... Understanding Oxygen Toxicity Part II: Hypotheses and Hyperoxia. Diver Alert Networks Reilly Fogarty examines the latest ... involves hyperoxia-induced free radical production overwhelming specific neural pathways, combined with localized neuron ... oblongata which is important in cardiorespiratory control and has some neurons that are particularly sensitive to hyperoxia and ...
Hyperoxia-induced formation of autophagosomes. The electron micrographs of retina in ROP model and control mice are showed in ... During the hyperoxia stage (from P8 to P13), the mRNA levels of Beclin1 (mammalian Atg6), Uncoordinated-51 like kinase 1 (ULK1 ... During the hyperoxia phase (P8-P12), the RNA expression of autophagic markers (ULK1, Beclin1, and Atg5) in retina was increased ... Hyperoxia and relative hypoxia not only cause retinal neovascularization, but also change the autophagy markers in the retina ...
The lungs of rhKGF-treated animals that survived hyperoxia exposure had minimal hemorrhage and no exudate within the ... Intratracheal instillation of keratinocyte growth factor decreases hyperoxia-induced mortality in rats. In: Journal of Clinical ... The lungs of rhKGF-treated animals that survived hyperoxia exposure had minimal hemorrhage and no exudate within the ... The lungs of rhKGF-treated animals that survived hyperoxia exposure had minimal hemorrhage and no exudate within the ...
Effects of hypo- and hyperoxia on transcription levels of five stress genes and the glutathione system in liver of Atlantic cod ... Effects of hypo- and hyperoxia on transcription levels of five stress genes and the glutathione system in liver of Atlantic cod ... Effects of hypo- and hyperoxia on transcription levels of five stress genes and the glutathione system in liver of Atlantic cod ... The transcript level of GSH-Px was significantly upregulated in fish exposed to hyperoxia, and significantly downregulated in ...
Exploring the risk of hyperoxia in oxygen-dependent very low birthweight infants in the first week of life to plan future ... Exploring the risk of hyperoxia in oxygen-dependent very low birthweight infants in the first week of life to plan future ... Because the haemoglobin oxygen dissociation curve flattens at higher SpO2, the likelihood of hyperoxia at higher SpO2 needs to ...
Results: Cell cycle regulatory genes were induced in Nrf2-/- lung at 1day of hyperoxia. At 3days of hyperoxia, induction of ... Results: Cell cycle regulatory genes were induced in Nrf2-/- lung at 1day of hyperoxia. At 3days of hyperoxia, induction of ... Results: Cell cycle regulatory genes were induced in Nrf2-/- lung at 1day of hyperoxia. At 3days of hyperoxia, induction of ... Results: Cell cycle regulatory genes were induced in Nrf2-/- lung at 1day of hyperoxia. At 3days of hyperoxia, induction of ...
Home/Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF Activation. Jain IH ... Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF Activation. Jain IH, ... Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF Activation. Jain IH, ... Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF Activation ...
In the present study, the lethal sensitivity to Legionella pneumonia were compared in the setting of hyperoxia between wild- ... mice were shown to be more resistant to Legionella-induced cytotoxicity than those from wild-type mice under hyperoxia. These ... signaling and apoptosis may be a crucial factor in the pathogenesis of Legionella pneumonia in the setting of hyperoxia. ... Hyperoxia accelerates Fas-mediated signaling and apoptosis in the lungs of Legionella pneumophila pneumonia. Access & Citations ...
The Validity of Retinal Blood Flow Measurements During Hyperoxia in Humans Using Fourier Domain Color Doppler Optical Coherence ... The Validity of Retinal Blood Flow Measurements During Hyperoxia in Humans Using Fourier Domain Color Doppler Optical Coherence ...
... Academic Article ... that occurs secondary to hyperoxia. In conclusion, inhaled NO administered with high concentrations of O2 may protect the lung ... whereas NO-derived oxidants may contribute to acute lung injury secondary to hyperoxia. Whether inhaled NO improves or ...
Hyperoxia was defined as any arterial oxygen value greater than 300 mmHg. Chi-square test was used to compare categorical ... Hyperoxia exposure was more common than previously reported and occurred more frequently in association with out-of-hospital ... Of these, 49 (41.2%) were exposed to hyperoxia and 70 (58.8%) were not during the first 24 hours after the CA. Those ... Statistical methods were used to identify predictors of hyperoxia exposure. Of 122 patients treated in the ICU following ...
... mesenchymal stem cells ameliorate experimental pulmonary hypertension induced by maternal inflammation and neonatal hyperoxia ... mesenchymal stem cells ameliorate experimental pulmonary hypertension induced by maternal inflammation and neonatal hyperoxia ...
Amelioration of Mitochondrial Dysfunction by Thioredoxin in Hyperoxia Das, Kumuda C. University of Texas Health Center at Tyler ... Although this toxicity is a key factor in the application of oxygen therapy, little is known about how hyperoxia impacts ... These findings propel us to hypothesize that Trx protects mitochondria from hyperoxia by reducing oxidative stress through UCP- ... Amelioration of Mitochondrial Dysfunction by Thioredoxin in Hyperoxia. Das, Kumuda C. / University of Texas Health Center at ...
Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia. Stephen G. Jenkinson, Richard A. Lawrence, Warren D ... Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia. In: Toxicological Sciences. 1984 ; Vol. 4, No. 2 ... Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia. Toxicological Sciences. 1984 Apr;4(2 PART1):170-177 ... Enhanced Pulmonary Toxicity in Copper-Deficient Rats Exposed to Hyperoxia. JENKINSON, S. G., LAWRENCE, R. A., GRAFTON, W. D., ...
Hemodynamic Effects of Prolonged Hyperoxia. MORAN, J. F.; WOLFE, W. G. MORAN, J. F.; WOLFE, W. G. Less ...
During each period, end-tidal PO2 was cycled between euoxia, hypoxia and hyperoxia, whilst the end-tidal PCO2 was maintained ... The acute ventilatory response to hypoxia (AHVR) was calculated as the difference in VE during hypoxia and hyperoxia within ... hypoxia and hyperoxia during rest and light exercise in humans. Three periods of ventilatory measurements were undertaken in ... Effect of raised potassium on ventilation in euoxia, hypoxia and hyperoxia at rest and during light exercise in man. ...
Hypoxia (12% O2) greatly reduced the chance of survival at 47.5°C, and hyperoxia greatly improved the chance of survival at ...
Whether hyperoxia affects the refraction in neonatal and adult mice is unknown. The mice exposed to 85% oxygen at postnatal 8 ... Effects of Hyperoxia on the Refraction in Murine Neonatal and Adult Models.. Mori, Kiwako; Kurihara, Toshihide; Jiang, Xiaoyan ... The neonatal hyperoxia group showed a significantly larger myopic change than the neonatal normoxia group (P47d -6.56 ± 5.89 D ... Postnatal 6 weeks (P6w) adult mice were divided into the adult hyperoxia and normoxia groups. These parameters were measured ...
The O2 regime controller for HyperOxia and HypOxia in the O2k. source ... Oxia - the O2 regime controller for HyperOxia and HypOxia in the O2k. October 26, 2021. OROBOROS INSTRUMENTS ... The O2 regime controller for HyperOxia and HypOxia in the O2k.. source ...
Lumb AB, Thomas C. Oxygen toxicity and hyperoxia. In: Lumb AB, ed. Nunn and Lumbs Applied Respiratory Physiology. 9th ed. ...
Effect of hyperoxia on vascular endothelial growth factor levels in a wound model. Arch Surg. 2000 Nov. 135(11):1293-7. [QxMD ... Effects of hyperoxia on neutrophil adhesion. Undersea Hyperb Med. 2004 Spring. 31(1):123-31. [QxMD MEDLINE Link]. ... bHyperoxia in normal tissues causes vasoconstriction, but this is compensated by increased plasma oxygen content and ... Hyperbaric hyperoxia enhances the lethal effects of amphotericin B in Leishmania braziliensis panamensis. Undersea Hyperb Med. ...
Enhanced Cerebral Blood Volume under Normobaric Hyperoxia in the J20-hAPP Mouse Model of Alzheimers Disease *Osman Shabir ...
The hyperoxia conditions were 85 percent oxygen. In room air, which is 21 percent oxygen, both the germ-free mice and non-germ- ... In general, Lal and colleagues found that germ-free mice had decreased hyperoxia-induced lung injury as compared to non-germ- ... Researchers study the effects of hyperoxia on the lung development of germ-free newborn mice. November 22, 2019. February 24, ... Dolma, K., et al. (2019) Effects of Hyperoxia on Alveolar and Pulmonary Vascular Development in Germ Free Mice. American ...
Kaneai N, Fukui K, Koike T, Urano S. Vitamin e prevents hyperoxia-induced loss of soluble n-ethylmaleimide- sensitive fusion ... Kaneai, N., Fukui, K., Koike, T., & Urano, S. (2013). Vitamin e prevents hyperoxia-induced loss of soluble n-ethylmaleimide- ... Kaneai, N, Fukui, K, Koike, T & Urano, S 2013, Vitamin e prevents hyperoxia-induced loss of soluble n-ethylmaleimide- ... Vitamin e prevents hyperoxia-induced loss of soluble n-ethylmaleimide- sensitive fusion protein attachment protein receptor ...
IHHT completed a 5-week program of exposure to hypoxia-hyperoxia while resting, CTRL completed an 8-week tailored exercise ... Intermittent Hypoxia-Hyperoxia Conditioning Improves Cardiorespiratory Fitness in Older Comorbid Cardiac Outpatients Without ... Aim: To compare a program based on intermittent hypoxia-hyperoxia training (IHHT) consisting of breathing hypoxic-hyperoxic gas ... Adaptations following an intermittent hypoxia-hyperoxia training in coronary artery disease patients: a controlled study → ...
  • Effect of raised potassium on ventilation in euoxia, hypoxia and hyperoxia at rest and during light exercise in man. (ox.ac.uk)
  • The purpose of this study was to determine whether changes in arterial plasma potassium concentration [K+]a affect expired ventilation (VE) in euoxia, hypoxia and hyperoxia during rest and light exercise in humans. (ox.ac.uk)
  • During each period, end-tidal PO2 was cycled between euoxia, hypoxia and hyperoxia, whilst the end-tidal PCO2 was maintained constant. (ox.ac.uk)
  • The acute ventilatory response to hypoxia (AHVR) was calculated as the difference in VE during hypoxia and hyperoxia within each period of measurement. (ox.ac.uk)
  • Development time, growth rate and fecundity were negatively impacted by both hypoxia and hyperoxia. (elsevier.com)
  • Its advantages include the early detection of hypoxia and hyperoxia, less frequent need for blood sampling for blood gas analysis, determination of the required fraction of inspiratory O2 and support for the process of ventilator weaning [1-3]. (who.int)
  • These experiments established that intratracheal administration of rhKGF stimulated alveolar type II cell proliferation in vivo and reduced hyperoxia-induced lung injury in rats. (northwestern.edu)
  • Pulmonary apoptosis in aged and oxygen-tolerant rats exposed to hyperoxia. (nih.gov)
  • The transcript levels of three genes coding for antioxidants, Cu/Zn superoxide dismutase (SOD), catalase and phospholipid hydroperoxide glutathione peroxidase (GSH-Px), and those of two stress proteins, metallothionein (MT) and CYP1A, were examined with real-time quantitative (q) RT-PCR in hepatic tissue of Atlantic cod exposed to 46% (hypoxia), 76% (normoxia) and 145% (hyperoxia) O-2 saturation (tank outlet). (nofima.no)
  • The transcript level of GSH-Px was significantly upregulated in fish exposed to hyperoxia, and significantly downregulated in fish exposed to hypoxia, compared to the normoxia group. (nofima.no)
  • The project is expected to provide a clear understanding of the way cytosolic Trx1 affects mitochondrial function during normoxia and hyperoxia. (grantome.com)
  • The mice exposed to 85% oxygen at postnatal 8 days (P8d) for 3 days and the mice exposed to normal air were assigned to the neonatal hyperoxia and normoxia groups, respectively. (bvsalud.org)
  • Postnatal 6 weeks (P6w) adult mice were divided into the adult hyperoxia and normoxia groups. (bvsalud.org)
  • The neonatal hyperoxia group showed a significantly larger myopic change than the neonatal normoxia group (P47d -6.56 ± 5.89 D, +4.11 ± 2.02 D, p (bvsalud.org)
  • however, the CR in the adult hyperoxia group was significantly smaller than the adult normoxia group (P12w, 1.44 ± 0.03 mm, 1.50 ± 0.03 mm, p = 0.003). (bvsalud.org)
  • The effects of training in hyperoxia vs normoxia on skeletal muscle enzyme activities and exercise performance. (gssiweb.org)
  • This theory suggests that exposure to high partial pressures of oxygen results in an increase in the firing rate of specific neurons, notably those of a part of the brain called the caudal Solitary Complex (cSC), a portion of the dorsal medulla oblongata which is important in cardiorespiratory control and has some neurons that are particularly sensitive to hyperoxia and pro-oxidants (Ciarlone, 2019). (gue.com)
  • 2019) Effects of Hyperoxia on Alveolar and Pulmonary Vascular Development in Germ Free Mice. (familiesdaily.com)
  • These findings propel us to hypothesize that Trx protects mitochondria from hyperoxia by reducing oxidative stress through UCP-2-dependent uncoupling, and furthermore by protecting mitochondrial dysfunction in hyperoxia as superoxide anion generation in the mitochondria is a key mechanism of pulmonary oxygen toxicity. (grantome.com)
  • To investigate the hypothesis that copper deficiency in the rat could result in decreased lung SOD activity and plasma ceruloplasmin concentration resulting in increased susceptibility to O 2 lung damage, we performed a series of experiments exposing copper-deficient and control rats to normobaric and hyperbaric hyperoxia. (unthsc.edu)
  • Further studies are needed to clarify the nonhematological adaptations to short, repeated exposure to normobaric hypoxia-hyperoxia. (aimediq.com)
  • Recent data suggests a decrease in cancer cell proliferation occurring after exposure to normobaric hyperoxia. (daneurope.org)
  • A generalized procedure for calibrated MRI incorporating hyperoxia and hypercapnia. (mpg.de)
  • Magnetic resonance imaging of resting OEF and CMRO₂ using a generalized calibration model for hypercapnia and hyperoxia. (mpg.de)
  • Hyperoxia exposure can inhibit alveolar growth in the neonatal lung through induction of p21/p53 pathways and is a risk factor for the development of bronchopulmonary dysplasia (BPD) in preterm infants. (elsevier.com)
  • We previously found that activation of nuclear factor erythroid 2 p45-related factor (Nrf2) improved survival in neonatal mice exposed to hyperoxia likely due to increased expression of anti-oxidant response genes. (elsevier.com)
  • It is not known however, whether hyperoxic induced Nrf2 activation attenuates the growth impairment caused by hyperoxia in neonatal lung. (elsevier.com)
  • To determine if Nrf2 activation modulates cell cycle regulatory pathway genes associated with growth arrest we examined the gene expression in the lungs of Nrf2 -/- and Nrf2 +/+ neonatal mice at one and 3days of hyperoxia exposure. (elsevier.com)
  • Methods: Microarray analysis was performed in neonatal Nrf2 +/+ and Nrf2 -/- lungs exposed to one and 3days of hyperoxia. (elsevier.com)
  • Sulforaphane, an inducer of Nrf2 was given to timed pregnant mice to determine if in utero exposure attenuated p21 and IL-6 gene expression in wildtype neonatal mice exposed to hyperoxia. (elsevier.com)
  • In utero SUL did not attenuate p21 expression in wildtype neonatal lung exposed to hyperoxia. (elsevier.com)
  • Effects of Hyperoxia on the Refraction in Murine Neonatal and Adult Models. (bvsalud.org)
  • Whether hyperoxia affects the refraction in neonatal and adult mice is unknown. (bvsalud.org)
  • In conclusion, hyperoxia was demonstrated to induce myopic shift both in neonatal and adult mice , which was attributed to the change in the CR rather than the AL. (bvsalud.org)
  • The lungs of rhKGF-treated animals that survived hyperoxia exposure had minimal hemorrhage and no exudate within the intraalveolar space. (northwestern.edu)
  • Directed delivery of KGF to the lungs may provide a therapeutic strategy to preserve or restore the alveolar epithelium during exposure to hyperoxia or other injurious agents. (northwestern.edu)
  • These findings suggest that although Nrf2 activation induces expression of anti-oxidant genes, it does not attenuate alveolar growth arrest caused by exposure to hyperoxia. (elsevier.com)
  • IHHT completed a 5-week program of exposure to hypoxia-hyperoxia while resting, CTRL completed an 8-week tailored exercise program, and participants in the CTRL were also exposed to sham hypoxia exposure. (aimediq.com)
  • Inhaled NO significantly attenuated the O2-mediated lung endothelial injury and abolished the increase in the bronchoalveolar lavage fluid content of rTI40, a specific and sensitive marker of alveolar epithelial type I cell injury, that occurs secondary to hyperoxia. (uab.edu)
  • The purpose of this research was to study the impact of hyperoxia on apoptosis and morphology of leukemia cell lines. (daneurope.org)
  • To test the hypothesis that KGFs effects ns type II cells in vivo might affect the response to lung injury, rats were treated with rhKGF and exposed to hyperoxia. (northwestern.edu)
  • Results: Cell cycle regulatory genes were induced in Nrf2 -/- lung at 1day of hyperoxia. (elsevier.com)
  • At 3days of hyperoxia, induction of cell cycle regulatory genes was similar in Nrf2 +/+ and Nrf2 -/- lungs, despite higher inflammatory gene expression in Nrf2 -/- lung. (elsevier.com)
  • Inhaled nitric oxide (NO) has been shown to prevent oxidant-induced lung injury in isolated-perfused lung models, whereas NO-derived oxidants may contribute to acute lung injury secondary to hyperoxia. (uab.edu)
  • Recently we published that increased expression of Thioredoxin protects the lung injury and increased survival of Trx-Tg mice in hyperoxia, but mice with lower expression of Trx were more sensitive to hyperoxia and suffered significant mortality. (grantome.com)
  • Although a medical necessity, high oxygen levels induce lung damage Our proposed studies will elucidate the protective mechanism of high levels of Thioredoxin, a cellular redox protein in hyperoxia-mediated lung injury. (grantome.com)
  • Charitharth Vivek Lal, M.D., and University of Alabama at Birmingham colleagues have used a novel and first-of-its-kind newborn mouse model to study the effect of high oxygen concentrations, or hyperoxia, on lung development of newborn mice that are germ-free - meaning no microbes colonizing their lungs. (familiesdaily.com)
  • Instead, we found that germ-free mice in hyperoxia showed protected lung structure, lung mechanics and decreased markers of inflammation compared to non-germ-free mice. (familiesdaily.com)
  • A structure that helps algae photosynthesize when carbon dioxide levels are low may also play a role during hyperoxia conditions. (elifesciences.org)
  • The team - which included researchers from Michigan State and ExxonMobil - found that a species of alga called Chlamydomonas reinhardtii contains pyrenoids when there are extremely high levels of oxygen in the air (also known as hyperoxia) despite carbon dioxide levels also being high ( Figure 1 ). (elifesciences.org)
  • to hypothesize that the signal that induces pyrenoid formation may be produced when photosynthesis takes place either under hyperoxia conditions or when there are low levels of carbon dioxide. (elifesciences.org)
  • These results suggest that hyperoxia induces a loss of SNARE proteins, which are involved in membrane docking between synaptic vesicles and pre-synaptic membranes, and that vitamin E prevents the oxidative damage of SNARE proteins. (elsevier.com)
  • We have now realized that the combined action of both hyperoxia (an excess of oxygen in the body) and hyperbaric pressure, leads to significant improvement in tissue oxygenation while targeting both oxygen and pressure sensitive genes, resulting in improved mitochondrial metabolism with anti-apoptotic (anti-cell death) and anti-inflammatory effects. (jpost.com)
  • Hyperoxia and relative hypoxia not only cause retinal neovascularization, but also change the autophagy markers in the retina of newborn mice. (researchsquare.com)
  • Our preliminary data establish that cytoplasmic Trx1 translocates to mitochondria during hyperoxia, but this movement does not occur in dnTrx-Tg mice. (grantome.com)
  • to the nucleus in Trx-Tg mice can protect against the mitochondrial dysfunction caused by hyperoxia. (grantome.com)
  • Using the transgenic mice (and cells derived from them) for in vivo and in vitro mechanistic studies, we expect to uncover mitochondrial mechanisms that are modulated by Trx1 during hyperoxia. (grantome.com)
  • For the current study, we hypothesized that the lungs of germ-free mice would have an exaggerated phenotypic response to hyperoxia compared to non-germ-free mice. (familiesdaily.com)
  • We speculate that the presence of predisposing pathogenic microbiota in non-germ-free and humanized mice may accentuate the proinflammatory cascade in hyperoxia, thus leading to a worse phenotype as compared to germ-free animals," Lal said. (familiesdaily.com)
  • The hyperoxia elevated tau expression in the cerebellum of wild-type mice by about 70 percent. (alzforum.org)
  • Aerobic efficiency is associated with the improvement in maximal power output during acute hyperoxia. (ki.se)
  • Although this toxicity is a key factor in the application of oxygen therapy, little is known about how hyperoxia impacts mitochondrial energy production, or the protein regeneration mechanisms that can offer protection from its effects. (grantome.com)
  • Here, the effects of vitamin E on hyperoxia-induced changes in the expressions of N-ethylmaleimide-sensitive factor (NSF) and soluble NSF-attachment protein α (α-SNAP) in the rat brain were analyzed. (elsevier.com)
  • The deleterious effects of hyperoxia are becoming more and more apparent. (umaryland.edu)
  • An additional mechanism proposes seizure onset as a result of hyperoxia induced enzyme inhibition, notably of Gama Amino Butyric Acid (GABA). (gue.com)
  • Durlinger et al in a prospective observational study demonstrated that an oxygen saturation 95% or less effectively limited the number of patients with hyperoxia (PaO2 of greater than 100 mm Hg). (umaryland.edu)
  • The adult hyperoxia group also showed a significantly larger myopic change (P12w, -7.20 ± 4.09 D, +7.52 ± 2.54 D, p (bvsalud.org)
  • Vitamin E significantly inhibited the decrease in the expression of NSF in rats subjected to hyperoxia. (elsevier.com)
  • Atmospheric oxygen has varied substantially over the Phanerozoic (the last 500 million years) with periods of both hyperoxia and hypoxia relative to today. (elsevier.com)
  • Elucidation of the mechanisms of hyperoxia and the application of this result to humans should be carried out in future studies. (bvsalud.org)
  • To compare a program based on intermittent hypoxia-hyperoxia training (IHHT) consisting of breathing hypoxic-hyperoxic gas mixtures while resting to a standard exercise-based rehabilitation program with respect to cardiorespiratory fitness (CRF) in older, comorbid cardiac outpatients. (aimediq.com)
  • We will also create a novel conditional Trx knockout mouse, a PGC1a-knockout mouse with increased or decreased expression of Trx to understand in vivo role of high levels of Trx on mitochondrial dysfunction in hyperoxia. (grantome.com)
  • Is recovery in hyperoxia after high intensity training in hypoxia an added value? (hdf.hr)
  • Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF Activation. (sablesys.com)
  • Hypoxia (12% O2) greatly reduced the chance of survival at 47.5°C, and hyperoxia greatly improved the chance of survival at 48.5°C. This finding expands the scope of the oxygen-supply model to a terrestrial, endothermic species, suggesting that oxygen supply generally limits the heat tolerance of embryos. (datadryad.org)
  • When rats were subjected to hyperoxia, the expression of both SNARE proteins was markedly decreased compared to normal rats. (elsevier.com)
  • During the hyperoxia stage (from P8 to P13), the mRNA levels of Beclin1 (mammalian Atg6), Uncoordinated-51 like kinase 1 (ULK1), and Autophagy 5 (Atg5) were increased. (researchsquare.com)
  • As with mev-1 , the gas-1 mutation also rendered animals hypersensitive to hyperoxia. (wormbase.org)
  • Early in the investigation, cyanide was suspected as the adulterant responsible for the atypical reactions because several patients had venous hyperoxia and lactic acidosis. (cdc.gov)
  • La présente étude sur les patients en soins intensifs néonataux a pour objectif de définir l'emplacement de la sonde oxymétrique afin d'obtenir les relevés les plus fiables et les plus précis de la saturation en oxygène (SpO2). (who.int)
  • Using state-of-the-art techniques that include mitochondrial flux analysis, EPR spectroscopy, biochemical enzymatic assay, and cutting-edge molecular approaches, we will dissect the role Trx1 plays in protecting the dysfunctional mitochondria in hyperoxia. (grantome.com)
  • Unlike some insect groups, cockroaches have not been reported to exhibit gigantism during the late Paleozoic period of hyperoxia. (elsevier.com)
  • The general mechanism for central nervous system (CNS) toxicity resulting in tonic-clonic seizures (convulsions involving both muscle stiffening and twitching or jerking) involves hyperoxia-induced free radical production overwhelming specific neural pathways, combined with localized neuron depolarization and hyperexcitability. (gue.com)