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.
Organic compounds that contain 1,2-diphenylethylene as a functional group.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
A publication issued at stated, more or less regular, intervals.
Individual's rights to obtain and use information collected or generated by others.
A quantitative measure of the frequency on average with which articles in a journal have been cited in a given period of time.
The use of statistical methods in the analysis of a body of literature to reveal the historical development of subject fields and patterns of authorship, publication, and use. Formerly called statistical bibliography. (from The ALA Glossary of Library and Information Science, 1983)
"The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.
The evaluation by experts of the quality and pertinence of research or research proposals of other experts in the same field. Peer review is used by editors in deciding which submissions warrant publication, by granting agencies to determine which proposals should be funded, and by academic institutions in tenure decisions.
A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL).
The noninvasive measurement or determination of the partial pressure (tension) of oxygen and/or carbon dioxide locally in the capillaries of a tissue by the application to the skin of a special set of electrodes. These electrodes contain photoelectric sensors capable of picking up the specific wavelengths of radiation emitted by oxygenated versus reduced hemoglobin.
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564)
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
A condition of decreased oxygen content at the cellular level.
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
Common foot problems in persons with DIABETES MELLITUS, caused by any combination of factors such as DIABETIC NEUROPATHIES; PERIPHERAL VASCULAR DISEASES; and INFECTION. With the loss of sensation and poor circulation, injuries and infections often lead to severe foot ulceration, GANGRENE and AMPUTATION.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
Restoration of integrity to traumatized tissue.
Anatomical and functional disorders affecting the foot.
The release of stem cells from the bone marrow into the peripheral blood circulation for the purpose of leukapheresis, prior to stem cell transplantation. Hematopoietic growth factors or chemotherapeutic agents often are used to stimulate the mobilization.

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 ...
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Narimanbekov I.O.; Rozycki H.J., 1992: Hyperoxic hyperventilation induced lung damage manifested within eight hours in a rabbit model
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 ...
Eduardo Bancalari, MD has won several academic and professional awards within the pediatrics and neonatology fields and is an author of The Newborn 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 ...
There are adverse effects involved with rat placement in hyperoxia condition. Hypercapnia is a condition where there is high ...
"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 ...
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 ...
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 ...
... also contributes to tissue injury following irradiation and hyperoxia, as well as in diabetes. Oxidative ...
Normobaric hyperoxia protects against demyelination in an experimental model of pattern III multiple sclerosis lesions. In: ( ...
Petersen C, Wetterslev J, Meyhoff CS (August 2018). "Perioperative hyperoxia and post-operative cardiac complications in adults ...
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. Patient SafetyNet is a remote monitoring and ...
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 ...
As part of eliminating the last of piece of evidence, Raghu (Assisted by his father) murders his aunt through hyperoxia. (In a ...
Millicovsky G, Johnston MC (September 1981). "Hyperoxia and hypoxia in pregnancy: simple experimental manipulation alters the ...
Differentiation between a right-to-left shunt and pulmonary disease is often aided clinically by the results of a hyperoxia ...
If hyperoxia or excess oxygen occurs in our body, our cellular metabolism produces several highly reactive forms of oxygen ...
吸入加压的氧气会导致人体组织中氧含量过高,从而形成高氧症(英语:hyperoxia)。暴露在高压氧气中的类型不同,人体所受到的影响也不同。人体短时间内暴露在高于大气中氧气分压的氧气中会导致中枢神经系统中毒,长时间
Hyperoxia - Exposure of tissues to abnormally high concentrations of oxygen.. *Hypoventilation training ...
Hyperoxia 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 patients cyanosis is due to lung ...
The change in practice to avoid hyperoxia is associated with a significant decrease in neonatal morbidity and does not have a ... Avoiding hyperoxia in infants < or = 1250 g is associated with improved short- and long-term outcomes J Perinatol. 2006 Nov;26( ... A change in practice was instituted in January 2003 with the objective of avoiding hyperoxia in preterm infants with target O2 ... Conclusions: The change in practice to avoid hyperoxia is associated with a significant decrease in neonatal morbidity and does ...
Postischemic hyperoxia reduces hippocampal pyruvate dehydrogenase activity.. Richards EM1, Rosenthal RE, Kristian T, Fiskum G. ...
Hyperoxia preconditioning: the next frontier in neurology?. Liu W1, Liu K, Tao H, Chen C, Zhang JH, Sun X. ... Hyperoxia preconditioning with normobaric or hyperbaric oxygen has been found to be protective in some diseases in several ... In the present short review, we briefly described the development, application and mechanisms of hyperoxia preconditioning in ... Currently, investigators pay increasing attention to the application of hyperoxia preconditioning in the prevention of common ...
... treatment with exogenous surfactant protein B improved survival and lung histology in Stat-3-deleted mice during hyperoxia. ...
Diseases : Hyperoxia, Lung Damage. Pharmacological Actions : Anti-Inflammatory Agents, Interleukin-6 Downregulation, Tumor ... Vitamin D seems to protect against hyperoxia-induced lung injury in newborn rats.Jun 12, 2016. ... Resveratrol could protect lungs from hyperoxia-induced injury through its antioxidant, anti-inflammatroy and anti-fibrotic ...
Resveratrol could protect lungs from hyperoxia-induced injury through its antioxidant, anti-inflammatroy and anti-fibrotic ... Resveratrol Attenuates Hyperoxia-induced Oxidative Stress, Inflammation and Fibrosis and Suppresses Wnt/β-catenin Signaling in ... In this study, the effect of resveratrol on the lung injury was evaluated in hyperoxia-exposed rats of preterm birth. The ... Furthermore, Wnt/β-catenin signaling was found active in hyperoxia-induced lungs. In addition, expression of SP-C was increased ...
Ventilatory effects of prolonged hyperoxia at pressures of 1.5-3.0 ATA. Aviat Space Environ Med 2006; 77:801-810.. Introduction ... early in hyperoxia at all exposure pressures persisted throughout hyperoxia, and reversed post-O2 exposure. Hyperventilation ... Discussion: Hyperoxia has concurrent toxic and physiological effects on respiratory control; degrees depend on O2 dose ( ... and after hyperoxia in a study of organ systems tolerance to toxic O2 exposures at 1.5 ATA (17.7 h), 2.0 ATA (9.3 h), 2.5 ATA ...
... William J. Mach,1 Amanda R. Thimmesch,1 J. Thomas Pierce,2 ... William J. Mach, Amanda R. Thimmesch, J. Thomas Pierce, and Janet D. Pierce, "Consequences of Hyperoxia and the Toxicity of ...
Habler, Oliver; Kleen, Martin; Kemming, Gregor und Zwissler, Bernhard (2002): Hyperoxia in extreme hemodilution. In: European ... The hyperoxia-associated microcirculatory dysregulation and impaired tissue oxygenation known to take place in the presence of ... hyperoxia). In experimental and clinical studies hyperoxic ventilation has emerged as a simple, safe and effective intervention ...
We agree that there are many potential risks associated with hyperoxia, including but not limited to reductions in coronary and ...
Hyperoxia had the opposite effect, resulting in a rapid reduction in cell growth. At 40 % hyperoxia, 1.3 and 2-fold decreases ... Hyperoxia-induced cell death through caspase-dependent pathways We then examined if hyperoxia-induced cell death was dependent ... Combined hyperoxia can significantly potentiate the anti-tumor effect of TMZ. Hyperoxia may attenuate TMZ resistance in GBM via ... We have adopted a different approach to modulation of hypoxia-mediated chemoresistance-use of induced hyperoxia. Hyperoxia has ...
Li Z, Choo-Wing R, Sun H, Sureshbabu A, Sakurai R, Rehan VK et al (2011) A potential role of the JNK pathway in hyperoxia- ... Hyperoxia cause adult rat lung fibroblast cultures to produce apparently autocrine growth factors. Exp Lung Res 14:403-419 ... Chen CM, Wang LF, Chou HC, Lang YD, Lai YP (2007) Up-regulation of connective tissue growth factor in hyperoxia-induced lung ... The primary culture of LFs from hyperoxia-exposed rats is a feasible method for studying the pathogenesis and treatment of lung ...
... *Download PDF Copy ... Jaap Jan Vos and colleagues sought to evaluate the correlation of ORi to PaO2 during moderate hyperoxia. They collected data ... It may help to better titrate oxygen therapy to avoid both hypoxia and unintended hyperoxia." ... relative indicator of a patients oxygen reserve during moderate hyperoxia. ORi can be trended and has optional alarms to ...
... Antioxid Redox Signal. 2008 Nov;10(11):1869-82. ... The deficiency in EPC mobilization is presumably due to impairment of eNOS-NO cascade in bone marrow (BM). Hyperoxia, induced ... Administration of exogenous SDF-1alpha into wounds reversed the EPC homing impairment and, with hyperoxia, synergistically ...
... clinicaltrials.gov Several studies show how patients with hyperoxia after cardiac arrest has increased mortality, but the ... Several studies show how patients with hyperoxia after cardiac arrest has increased mortality, but the association of hyperoxia ... Hyperoxia Before and After Cardiac Arrest and Myocardial Damage. 2019-07-10 20:05:50 , BioPortfolio ... More From BioPortfolio on "Hyperoxia Before and After Cardiac Arrest and Myocardial Damage". *Related Companies*Related ...
Hyperoxia in body tissues is produced by breathing high concentrations of molecular oxygen. This may cause oxygen toxicity, one ... Retrieved from "https://www.biology-online.org/dictionary/index.php?title=Hyperoxia&oldid=95352" ...
Hyperoxia: An abnormal increase in the amount of oxygen in the tissues and organs. ... hyperoxia during occlusion is beneficial in promoting recovery from arterial occlusion, and (3) hyperoxia has value even if it ... hyperoxia for 24 hours followed by mechanical ventilation for 4 hours. ". 03/01/2014 - "Hyperoxia and the mechanical load ... which was reduced by hyperoxia, but to local retinal ganglion cell layer-derived VEGF. ". 06/01/2015 - "Hyperoxia exposure led ...
Bronchopulmonary dysplasia Hyperoxia Newborn Pulmonary hypertension Pulmonary microvascular disease Electronic supplementary ... Warner BB, Stuart LA, Papes RA et al (1998) Functional and pathological effects of prolonged hyperoxia in neonatal mice. Am J ... Bucher JR, Roberts RJ (1981) The development of the newborn rat lung in hyperoxia: a dose-response study of lung growth, ... Li C, Fu J, Liu H et al (2014) Hyperoxia arrests pulmonary development in newborn rats via disruption of endothelial tight ...
Hyperoxia did not alter the expression level of NALP3 or ASC (Fig. 5A). However, hyperoxia enhanced the interaction between ASC ... Apyrase inhibited hyperoxia-induced release of IL-1β. To test whether hyperoxia-induced autocrine ATP release is responsible ... Hyperoxia enhances the interaction among inflammasome components. Mice were exposed to hyperoxia (100% O2) for various time ... The NAC significantly inhibited IL-1β maturation in response to hyperoxia (Fig.7), suggesting that in addition to K+, hyperoxia ...
Hyperoxia may increase the risk of developing lung injury (hyperoxia-induced lung injury - HALI), which carries a high ... A direct influence of hyperoxia with an increase in systemic vascular resistance has also been suggested, and hyperoxia may not ... GLP-1 and Hyperoxia for Organ Protection in Heart Surgery (GLORIOUS). The safety and scientific validity of this study is the ... Hyperoxia during and after ischemia has been investigated in several settings, and a final consensus of its benefits and ...
Atelectasis Formation: Role of Positive Pressure Breathing, Hyperoxia, and Hypobaria. The safety and scientific validity of ... Hyperoxia. Lung Diseases. Respiratory Tract Diseases. Signs and Symptoms, Respiratory. Signs and Symptoms. ... Influence of Hyperoxia and Hypobaria on Atelectasis Occurrence and Mitigation of Atelectasis Formation. ... The effect of positive pressure breathing on lung function is being studied, when applied during exposure to hyperoxia and +Gz- ...
To investigate a chronic lung disease, image classification in the cloud was used to distinguish between healthy and diseased lungs.
Looks like divers arent the only ones who need to be aware of hyperoxia: NASA Decodes Trouble With F-22 Issue has actually ... Hyperoxia- not just for divers anymore! Looks like divers arent the only ones who need to be aware of hyperoxia:. NASA Decodes ... Re: Hyperoxia- not just for divers anymore! Maybe they need a BOV just in case they get any symptoms? ... Re: Hyperoxia- not just for divers anymore! "absorption atelectasis, in which too much oxygen can wash away necessary nitrogen ...
... generated during hyperoxia. The aim of this study was to investigate the role of ROS in ... Hyperoxia can cause substantial reductions in peripheral and coronary blood flow at rest and during exercise, which may be ... In the sub-group that demonstrated the greatest hyperoxia-induced changes (, 20%), FBF and FVC during hyperoxia were 67.1±4.0% ... generated during hyperoxia. The aim of this study was to investigate the role of ROS in hyperoxia-induced reductions in ...
... style="width:100%;"> ... Tikhonov, M., Baranov, V., and Kotov, A., "Immersion, Hyperoxia, Hypercapnia: Additive Effect Upon Pulmonary Function," SAE ... we did non find any potentiation of oxygen induced toxic effects upon the lungs during immersion/hyperoxia/hypercapnia ...
PROTECTIVE EFFECT OF N-ACETYLCYSTEINE ON HYPEROXIA-INDUCED LUNG INJURY AND ITS INTERACTION WITH P38 MITOGEN-ACTIVATED PROTEIN ... PROTECTIVE EFFECT OF N-ACETYLCYSTEINE ON HYPEROXIA-INDUCED LUNG INJURY AND ITS INTERACTION WITH P38 MITOGEN-ACTIVATED PROTEIN ... PROTECTIVE EFFECT OF N-ACETYLCYSTEINE ON HYPEROXIA-INDUCED LUNG INJURY AND ITS INTERACTION WITH P38 MITOGEN-ACTIVATED PROTEIN ... PROTECTIVE EFFECT OF N-ACETYLCYSTEINE ON HYPEROXIA-INDUCED LUNG INJURY AND ITS INTERACTION WITH P38 MITOGEN-ACTIVATED PROTEIN ...
Bitterman H., Brod V., Bitterman N. (1998) Hemodynamic Effects of Hyperoxia in Hemorrhagic Shock. In: Gullo A. (eds) ...
  • Hyperoxia occurs when cells, tissues and organs are exposed to an excess supply of oxygen (O2) or higher than normal partial pressure of oxygen. (wikipedia.org)
  • This kind of hyperoxia can lead to oxygen toxicity, caused from the harmful effects of breathing molecular oxygen at elevated partial pressures. (wikipedia.org)
  • hyperoxia refers to a state in which oxygen supply is excessive, and hypoxia refers to a state in which oxygen supply is insufficient. (wikipedia.org)
  • Associated with hyperoxia is an increased level of reactive oxygen species (ROS), which are chemically reactive molecules containing oxygen. (wikipedia.org)
  • These guidelines stress the use of 28% oxygen masks and caution the dangers of hyperoxia. (wikipedia.org)
  • Breathing nitrox can lead to hyperoxia due to the high partial pressure of oxygen if used too deep or for too long. (wikipedia.org)
  • The highest risk of hyperoxia is in hyperbaric oxygen therapy, where it is a high probability side effect of the treatment for more serious conditions, and is considered an acceptable risk as it can be managed effectively without apparent long term effects. (wikipedia.org)
  • Hyperoxia preconditioning with normobaric or hyperbaric oxygen has been found to be protective in some diseases in several animal models and clinical trials. (nih.gov)
  • Although survival rate of infants born prematurely has been raised by supplemental oxygen treatment, it is followed by high morbidity of hyperoxia-induced bronchopulmonary dysplasia. (greenmedinfo.com)
  • Beside red blood cell transfusion, arterial oxygen content can be rapidly increased by ventilating the patient with 100% oxygen (hyperoxic ventilation), thus enhancing the amount of physically dissolved oxygen in plasma (hyperoxia). (uni-muenchen.de)
  • We agree that there are many potential risks associated with hyperoxia, including but not limited to reductions in coronary and cerebral blood flow, decreased cardiac output, increased oxidative stress, delay in recognising a clinical deterioration and rebound hypoxaemia if oxygen therapy is abruptly stopped. (bmj.com)
  • ORi is available outside the U.S. and is intended as a noninvasive, relative indicator of a patient's oxygen reserve during moderate hyperoxia. (news-medical.net)
  • It may help to better titrate oxygen therapy to avoid both hypoxia and unintended hyperoxia. (news-medical.net)
  • Hyperoxia, induced by a clinically relevant hyperbaric oxygen therapy (HBO) protocol, can significantly enhance the mobilization of EPCs from the BM into peripheral blood. (nih.gov)
  • Hyperoxia in body tissues is produced by breathing high concentrations of molecular oxygen . (biology-online.org)
  • In the 6 studies, high-concentration oxygen therapy resulted in hyperoxia, with a range in mean Pao(2) of 273 to 425 mm Hg. (curehunter.com)
  • however, it is known that high levels of inspired fraction of oxygen result in regionally decreased perfusion in the brain potentially confounding the possibility of using hyperoxia as a means of measuring blood flow and volume. (curehunter.com)
  • To test this hypothesis, we characterized the expression and activation of inflammasome components in primary murine alveolar macrophages exposed to hyperoxia (95% oxygen and 5% CO 2 ) in vitro, and in alveolar macrophages isolated from mice exposed to hyperoxia (100% oxygen). (jimmunol.org)
  • Hyperoxia can cause substantial reductions in peripheral and coronary blood flow at rest and during exercise, which may be caused by reactive oxygen species (ROS) generated during hyperoxia. (biomedsearch.com)
  • Contrary to our expectation, we did non find any potentiation of oxygen induced toxic effects upon the lungs during immersion/hyperoxia/hypercapnia exposures. (sae.org)
  • Supraphysiological concentrations of oxygen (hyperoxia) can compromise host defense and increase susceptibility to bacterial infections, causing ventilator-associated pneumonia. (ovid.com)
  • The phagocytic activity of macrophages is impaired by hyperoxia-induced increases in the levels of reactive oxygen species (ROS) and extracellular high-mobility group box protein B1 (HMGB1). (ovid.com)
  • BIRMINGHAM, Ala. - 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. (brightsurf.com)
  • The hyperoxia conditions were 85 percent oxygen. (brightsurf.com)
  • To investigate the effects of hyperoxia on retinal oxygenation and oxygen consumption in the detached feline retina. (arvojournals.org)
  • The present work suggests that hyperoxia is protective because it allowed increased photoreceptor oxygen consumption. (arvojournals.org)
  • Whereas normal P o 2 s were maintained at the inner and outer border of the avascular region during hyperoxia, Q av was not restored to normal, suggesting that other factors are involved in photoreceptor dysfunction during detachment in addition to insufficient oxygen delivery. (arvojournals.org)
  • Although the beneficial effects of hyperoxia have been demonstrated histologically, and a theoretical explanation has been proposed, there are no oxygen data available to validate the theory or assess the extent of protection that hyperoxia might afford. (arvojournals.org)
  • Young adult C57BL/6J mice raised in dim cyclic illumination (12 h at 5 lx and 12 h in darkness) were exposed to hyperoxia (75% oxygen for two weeks). (molvis.org)
  • The animals were under general anesthesia during hyperoxia (100% oxygen) for 10 minutes 24 hours after intravitreal injection of L-2-aminoadipic acid (LAA), a gliotoxic compound, or diluted hydrochloric acid (0.01 N) used as the vehicle control. (arvojournals.org)
  • On another day, measurements were repeated at a second baseline (B2) and during hyperoxia (100% oxygen breathing) for 15 normal subjects and 13 glaucoma patients. (bmj.com)
  • Adaptive Tolerance to Pulmonary Oxygen Toxicity After Hypoxia or Intermittent Hyperoxia. (annals.org)
  • Hyperoxia is present in many anaesthesia protocols used in animal blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) studies. (tu-darmstadt.de)
  • Using an established model of prematurity-related lung disease, pups from timed-pregnant Sprague Dawley rats were randomized to normoxia or hyperoxia (fraction of inspired oxygen, 0.85) exposure for the first 14 days of life. (ovid.com)
  • 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). (spandidos-publications.com)
  • We hypothesize that consequences of hyperoxia may also be developmentally regulated and mitochondrial reactive oxygen species (ROS) dependent. (luriechildrens.org)
  • To determine whether age of exposure impacts the effect of hyperoxia, neonatal mice were placed in 75% oxygen for 72 h at either postnatal day 0 (early postnatal) or day 4 (late postnatal). (luriechildrens.org)
  • who hypothesized that its pathogenesis stemmed from prolonged mechanical ventilation of the surfactant-deficient lung with high concentrations of inspired oxygen (hyperoxia) [ 1 ]. (biomedcentral.com)
  • At high fractions and prolonged exposure, hyperoxia may lead to excessive generation of reactive oxygen intermediates overwhelming cellular antioxidant defence and inducing oxidative damage. (eestiarst.ee)
  • Hyperoxia may affect a variety of patients' biological systems, such as antioxidant enzymes [ 9 ] and cytokine production [ 10 ] through excessive production of reactive oxygen species. (biomedcentral.com)
  • Using the keywords of "hyperoxia" or "oxygenation target" or "hyperoxemia" or "oxygen saturation" or "arterial oxygen" and "critically ill" or "intensive care" or "mechanical ventilation", we conducted a comprehensive computer search in Pubmed, Embase, Medline, Cochrane Central Register of Controlled Trails (CENTRAL) and Information Sciences Institute (ISI) Web of Science from 1946 to December 2016 regardless of publication types or language. (biomedcentral.com)
  • Female A/J mice were given a single dose of B[a]P and randomized into four groups: control, carboplatin (50 mg/kg intraperitoneally), hyperoxia (95% fraction of inspired oxygen), and carboplatin and hyperoxia. (kjim.org)
  • Hyperoxia may impair oxygen delivery in patients with sepsis, and hyperoxia decreases whole-body oxygen consumption in critically ill patients (2,6). (wikidot.com)
  • This episode concentrates on hyperoxia - the delivery of lots (often too much) oxygen and the harms it may cause our patients. (phemcast.co.uk)
  • If I injured my brain I think I'd have some oxygen, please - I'd chance the potential harm of hyperoxia to make as sure as possible that I didn't suffer any spells of hypoxia, until transport monitoring is infallible. (phemcast.co.uk)
  • Since a prolonged excessive oxygen concentration poses the risk of long-term adverse alterations in the lung architecture and pulmonary function [ 6 ], prevention of hyperoxia-induced lung injury is still an issue with major importance. (biomedcentral.com)
  • Its excess of oxidative radical products in hyperoxia mediate adverse effects of oxygen. (biomedcentral.com)
  • However, several studies published recently have questioned the routine use of high inspired oxygen concentration (hyperoxia) to improve oxygen delivery, specifically in the neonatal period but possibly even following myocardial infarction. (clinicaltrials.gov)
  • ABSTRACT Title: The risk for hyperoxia after extra oxygen therapy for apnea in preterm infants Introduction: Preterm infants with apnea's combined with bradycardia and cyanosis (ABC), often receive extra oxygen. (uu.nl)
  • It is known that extra oxygen therapy increases the risk for hyperoxia. (uu.nl)
  • Aim: To investigate occurrence and duration of hyperoxia after extra oxygen for ABC's and how this is related to the duration of bradycardia and/or cyanosis. (uu.nl)
  • Research questions: What is the occurrence and duration of hyperoxia in preterm infants treated with extra oxygen given after an ABC and how long last hyperoxia when compared to the duration of bradycardia and cyanosis and how are these correlated? (uu.nl)
  • Hyperoxia lasted longer after ABC's when infants received ambient air than when extra oxygen was given before ABC occurred. (uu.nl)
  • Conclusion: In preterm infants supported with nCPAP, hyperoxia after extra oxygen supply for ABC's was frequent and lasted longer than bradycardia and cyanosis during ABC. (uu.nl)
  • Jackson, RM & Pisarello, JB 1984, ' The endotoxin-pretreated, oxygen-adapted rat model in hyperbaric hyperoxia ', Aviation Space and Environmental Medicine , vol. 55, no. 8, pp. 709-714. (elsevier.com)
  • Our results offer new perspectives on the effects and the mechanism of exogenous surfactant in protecting the airway and lungs, in oxygen-rich lung microenvironment, against oxidative damage and aggravation of acute inflammation induced by hyperoxia. (springeropen.com)
  • Patients who received hyperoxia during general surgery had an increase in surgical site infections compared to those who received a lower oxygen concentration. (reliasmedia.com)
  • In cultured human lung epithelial cells, exposure to hyperoxia alone (95% oxygen) did not affect NF-κB activation or degradation of the NF-κB inhibitory protein, IκBα. (northwestern.edu)
  • however, perfusion changes at all oxygen levels were relatively mild (less than 10%) supporting the viability of hyperoxia-induced contrast. (ox.ac.uk)
  • Objectives: To explore the relationship between early hypoxia and hyperoxia on outcome from TBI. (ahajournals.org)
  • Conclusions: Both hypoxia and hyperoxia were associated with increased mortality in TBI patients, even after adjusting for multiple factors affecting outcomes. (ahajournals.org)
  • 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," Lal said. (brightsurf.com)
  • Consistently, the response to hyperoxia was an increased perfusion in the ischemic limb and decreased perfusion in the contralateral limb. (inserm.fr)
  • Leptin deficiency abolishes the response to hyperoxia, which is restored by leptin replacement. (elsevier.com)
  • Cerebral perfusion response to hyperoxia. (ox.ac.uk)
  • Resveratrol intraperitoneal administration alleviated hyperoxia-induced histological injury of lungs, regulated redox balance, decreased pro-inflammatory cytokines release, and down-regulated expression of fibrotic-associated proteins. (greenmedinfo.com)
  • The ultrastructure of pulmonary microvasculature in the hyperoxia-exposed lungs revealed a collapsed capillary lumen. (springer.com)
  • Although cardiac index was similar, hyperoxia-exposed rats demonstrated a reduced RV ejection fraction and significant RV-pulmonary vascular uncoupling. (ovid.com)
  • KGF decreases mortality in hyperoxia-exposed newborn rodents, a classic model of injury-induced impaired alveolarization, although the pulmonary mechanisms of this protection are poorly defined. (physiology.org)
  • Mice exposed to early, but not late, postnatal hyperoxia demonstrated decreased alveolarization and septation, increased muscularization of resistance pulmonary arteries, and right ventricular hypertrophy (RVH) compared with normoxic controls. (luriechildrens.org)
  • In conclusion metformin prolongs survival and attenuates pulmonary injury by reducing pulmonary inflammation, coagulation, and fibrosis but does not affect alveolar development or prevent pulmonary arterial hypertension and right ventricular hypertrophy in neonatal rats with severe hyperoxia-induced experimental BPD. (physiology.org)
  • Large-tidal volume (V T ) mechanical ventilation and hyperoxia used in patients with acute respiratory distress syndrome can damage pulmonary epithelial cells through lung inflammation and apoptotic cell death. (biomedcentral.com)
  • Early hyperoxia exposure led to a significant increase in NOS3 (median fold change × 2.37, IQR 1.54-3.68) and STAT3 (median fold change × 2.83, IQR 2.21-3.88) mRNA levels in pulmonary endothelial cells with corresponding changes in histone modification patterns such as H2aZac and H3K9ac hyperacetylation at the respective gene loci. (biomedcentral.com)
  • Resveratrol could protect lungs from hyperoxia-induced injury through its antioxidant, anti-inflammatroy and anti-fibrotic effects. (greenmedinfo.com)
  • Resveratrol Attenuates Hyperoxia-induced Oxidative Stress, Inflammation and Fibrosis and Suppresses Wnt/β-catenin Signaling in Lungs of Neonatal Rats. (greenmedinfo.com)
  • Furthermore, Wnt/β-catenin signaling was found active in hyperoxia-induced lungs. (greenmedinfo.com)
  • In addition, expression of SP-C was increased and T1α was decreased in hyperoxia-exposed lungs. (greenmedinfo.com)
  • To find a better model for studying the role of LFs in hyperoxia-induced lung fibrosis at the cellular level, we isolated LFs from the lung tissue of hyperoxia- and normoxia-exposed rat lungs on postnatal days 7, 14 and 21 for primary culture to study their proliferative behavior. (springer.com)
  • Hyperoxia exposure to developing lungs-critical in the pathogenesis of bronchopulmonary dysplasia-may augment lung inflammation by inhibiting anti-inflammatory mediators in alveolar macrophages. (hindawi.com)
  • We observed an increased expression of miR-184 in BPD clinical specimens: tracheal aspirates (TA), human neonatal lungs with BPD and in fetal human lung Type II alveolar epithelial cells (TIIAECs) exposed to hyperoxia. (ersjournals.com)
  • Consistent with this, we also detected an upregulated miR-184-3p expression in whole lungs, in freshly isolated TIIAECs from lungs of hyperoxia-induced experimental BPD mice and in fetal mice lung TIIAECs exposed to hyperoxia. (ersjournals.com)
  • Hyperoxia causes miR-34a-mediated injury via angiopoietin-1 in neonatal lungs. (jefferson.edu)
  • Here we show that lung micro-RNA (miR)-34a levels are significantly increased in lungs of neonatal mice exposed to hyperoxia. (jefferson.edu)
  • No complete restoration in histone signatures at these loci was observed, and responsivity to later hyperoxia was altered in mouse lungs. (biomedcentral.com)
  • Normobaric hyperoxia preconditioning has been demonstrated to induce neuroprotection in rats. (spandidos-publications.com)
  • 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. (spandidos-publications.com)
  • Normobaric hyperoxia preconditioning improved prolonged escape latency and raised the number of platform crossings induced by sevoflurane in the Morris water maze test, increased the level of bcl‑2 protein, and decreased the level of bax and active caspase‑3 protein, the apoptosis rate and cytosolic calcium concentration in the hippocampus 24 h after sevoflurane exposure. (spandidos-publications.com)
  • The findings of the present study may imply that normobaric hyperoxia preconditioning attenuates sevoflurane‑induced spatial learning and memory impairment, and this effect may be partly related to apoptosis inhibition in the hippocampus. (spandidos-publications.com)
  • In conclusion, normobaric hyperoxia preconditioning may be a promising strategy against sevoflurane‑induced cognitive impairment by inhibiting the hippocampal neuron apoptosis. (spandidos-publications.com)
  • We explored the effects of intermittent normobaric hyperoxia alone or combined with chemotherapy on the growth, general morphology, oxidative stress, and apoptosis of benzo[a]pyrene (B[a]P)-induced lung tumors in mice. (kjim.org)
  • Normobaric hyperoxia (95%) was applied for 3 hours each day from weeks 21 to 28. (kjim.org)
  • Intermittent normobaric hyperoxia combined with chemotherapy reduced the tumor number by 59% and the load by 72% compared with the control B[a]P group. (kjim.org)
  • Intermittent normobaric hyperoxia, either alone or combined with chemotherapy, decreased the levels of superoxide dismutase and glutathione and increased the levels of catalase and 8-hydroxydeoxyguanosine. (kjim.org)
  • Intermittent normobaric hyperoxia was found to be tumoricidal and thus may serve as an adjuvant therapy for lung cancer. (kjim.org)
  • We explored whether intermittent normobaric hyperoxia was tumoricidal in mice with lung tumors and whether hyperoxia enhanced the effect of carboplatin chemotherapy. (kjim.org)
  • The influence of normobaric hyperoxia on lung surfactant phosp. (mysciencework.com)
  • The influence of 12-, 24- and 48-h normobaric hyperoxia on phospholipid composition of lung surfactant in rats was investigated. (mysciencework.com)
  • These data suggest that normobaric hyperoxia causes a substantial changes in lung surfactant composition and type II pneumocyte metabolism. (mysciencework.com)
  • Delayed hyperbaric oxygenation is more effective than early prolonged normobaric hyperoxia in experimental focal cerebral ischemia. (qxmd.com)
  • The patients will undergo three sessions of hyperoxia therapy in the hyperbaric chamber situated at the BUPA Hospital, Anlaby Road, Hull. (isrctn.com)
  • Exposure to hyperoxia for a limited time before ischaemia induces a low-grade oxidative stress and evokes an (ischaemic) preconditioning-like effect in the myocardium, which protects the heart from subsequent injury. (eurekaselect.com)
  • Our prior work in murine models identified postnatal maturation of antioxidant enzyme capacities as well as developmental regulation of mitochondrial oxidative stress in hyperoxia. (luriechildrens.org)
  • Oxidative stress and its effects on DNA are increased following exposure to hyperoxia and even more with chemotherapy, and this may lead to apoptosis of lung tumors. (kjim.org)
  • Our results showed that TMZ sensitivity of both chemo-sensitive and resistant cells was enhanced significantly under hyperoxia. (biomedsearch.com)
  • The LFs isolated from rats exposed to hyperoxia in vivo showed significantly greater proliferation than that from normoxia-exposed rats. (springer.com)
  • In addition, when ATP was scavenged with apyrase, hyperoxia-induced inflammasome activation was significantly decreased. (jimmunol.org)
  • In addition, BRP-39 −/− mice were significantly more sensitive to LPS plus hyperoxia induced lung injury and mortality compared to WT mice. (hindawi.com)
  • hyperoxia increased it to a level that was not significantly different from the control (attached retina, air breathing). (arvojournals.org)
  • hyperoxia significantly increased the level. (arvojournals.org)
  • Aged hyperoxia-exposed rats developed significantly greater RV hypertrophy, associated with a 40% increase in RV systolic pressures. (ovid.com)
  • HIF-1α expression in the developing kidney was significantly reduced following hyperoxia exposure. (monash.edu)
  • 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. (elsevier.com)
  • Hyperoxia alone did not induce IκB kinase (IKK) activity, but significantly prolonged TNFα-mediated activation of IKK activity. (northwestern.edu)
  • 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. (jefferson.edu)
  • The results demonstrated that hyperoxia led to thickened alveolar wall, simplified alveolar architecture and fibrosis. (greenmedinfo.com)
  • This study focuses on the mechanisms of inflammasome activation by hyperoxia and the contributions of inflammasome activation to lung injury and alveolar epithelial permeability. (jimmunol.org)
  • BMP9 treatment of rat pups with hyperoxia-induced experimental BPD reduced alveolar enlargement, lung septal thickness and fibrosis, and prevented inflammation, but did not attenuate vascular remodeling and RVH. (frontiersin.org)
  • BMP9 protects against neonatal hyperoxia-induced BPD by improving aberrant alveolar development, inflammation and fibrosis, demonstrating its therapeutic potential for premature infants with severe BPD. (frontiersin.org)
  • Hyperoxia decreased by 30% the rate of wound closure of a monolayer of fetal alveolar epithelial cells, due to cell death, which was overcome by recombinant human KGF (100 ng/ml). (physiology.org)
  • After daily metformin treatment rat pups with experimental BPD had reduced mortality, alveolar septum thickness, lung inflammation, and fibrosis, demonstrated by a reduced influx of macrophages and neutrophils and hyperoxia-induced collagen III and fibrin deposition (25 mg/kg), as well as improved vascularization (100 mg/kg) compared with control treatment. (physiology.org)
  • In newborn mice, prolonged hyperoxia induces an arrest of alveolar development similar to that seen in human neonates with BPD. (biomedcentral.com)
  • In this regard, the murine hyperoxia model may provide an ideal alternative to study the pathologic arrest of alveolar development in BPD. (biomedcentral.com)
  • Neither has the association between hyperoxia after cardiac arrest and myocardial injury. (bioportfolio.com)
  • Our research hypothesis is that hyperoxia before cardiac arrest aggravates myocardial damage, secondly we wish to analyze the association between hyperoxia after cardiac arrest and myocardial injury. (bioportfolio.com)
  • Association Between Hyperoxia and Mortality After Stroke. (phemcast.co.uk)
  • We hypothesized that hyperoxia-induced K + efflux activates the inflammasome via the purinergic P2X7 receptor to cause inflammation and hyperoxic acute lung injury. (jimmunol.org)
  • However, prolonged exposure to hyperoxia leads to inflammation and acute lung injury (ALI) ( 1 - 3 ). (jimmunol.org)
  • 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. (brightsurf.com)
  • After hyperoxia-induced photoreceptor degeneration had begun, the number of genes that showed significant expression differences between the inferior and superior retina more than quadrupled, with genes related to immune processes, defense processes, and inflammation being numerically dominant. (molvis.org)
  • 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. (biomedcentral.com)
  • These findings suggest that stimulating the NO pathway by sildenafil and VIP exert their beneficial effect against hyperoxia-induced BHR via preserving normal EELV, inhibiting airway inflammation and preserving the physiological lung structure, whereas the antiapoptotic potential of these treatments were not apparent in this process. (biomedcentral.com)
  • In LPS-induced lung inflammation in association with hyperoxia, depressed PC synthesis and enhanced proinflammatory cytokine production may be alleviated by iNO. (biomedcentral.com)
  • Compared to the hyperoxia group, the administration of exogenous surfactant was able to reduce lung inflammation through a reduction in the influx of neutrophils and inflammatory biomarkers such as TNF, IL-17, and HMGB1 expression. (springeropen.com)
  • None of these experimental models, however, was originally designed to investigate in vivo the combined effects of surfactant on hyperoxia-induced inflammation. (springeropen.com)
  • Aged rats exposed to postnatal hyperoxia recapitulate many features of young adults born prematurely, including increased RV hypertrophy and decreased RV ejection fraction. (ovid.com)
  • Our data suggest that postnatal hyperoxia exposure results in mitochondrial dysregulation that persists into adulthood with eventual RV dysfunction. (ovid.com)
  • Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline. (semanticscholar.org)
  • Treatment with a mitochondria-specific antioxidant, (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphoniu m chloride (mitoTEMPO), during early postnatal hyperoxia protected against compromised alveolarization and RVH. (luriechildrens.org)
  • In addition, early, but not late, postnatal hyperoxia resulted in induction of NOX1 expression that was mitochondrial ROS dependent. (luriechildrens.org)
  • Hyperoxia and tumor necrosis factor-α (TNFα) are two canonical signals centrally involved in the patho-physiology of acute lung injury. (northwestern.edu)
  • Effect of acute hyperoxia on the bronchodilator response to salbutamol in stable asthmatic patients. (bmj.com)
  • This study was designed therefore to examine the effect of acute hyperoxia (Fio2 1.0) on the bronchodilator response to salbutamol in stable asthmatic patients. (bmj.com)
  • This study compares the effect of acute hyperoxia on blood pressure and heart rate variability between hypertensive and normotensive subjects. (viamedica.pl)
  • The purpose of the present study was to examine the effects of hyperoxia exposure (HP) on free radicals (FR) accumulation in relation to the ultrastructural pathological alterations in the diaphragm. (omicsonline.org)
  • The present study was undertaken to further examine the effects of hyperoxia in this patient population. (reliasmedia.com)
  • Angiotensin II type 2 receptor ligand PD123319 attenuates hyperoxia-induced lung and heart injury at a low dose in newborn rats. (sigmaaldrich.com)
  • Recent studies in patients after cardiac arrest and traumatic brain injury have suggested that hyperoxia is associated with worse outcomes. (bmj.com)
  • This review addresses the effects of pretreatment by hyperoxia both in experimental and clinical setting. (eurekaselect.com)
  • Conclusions In SAH patients, exposure to hyperoxia was associated with DCI. (bmj.com)
  • Conclusions Results of the study indicate that deactivation of carotid bodies with hyperoxia decreases sympathetic activity measured using blood pressure variability method. (viamedica.pl)
  • Effects of hypoxia, hyperoxia, and hypercapnia on baseline and stimulus-evoked BOLD, CBF, and CMRO2 in spontaneously breathing animals. (harvard.edu)
  • Several studies show how patients with hyperoxia after cardiac arrest has increased mortality, but the association of hyperoxia before cardiac arrest and myocardial damage has never been investigated. (bioportfolio.com)
  • Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. (biomedcentral.com)
  • 400 mmHg, hyperoxia had no independent association with mortality. (biomedcentral.com)
  • Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. (biomedcentral.com)
  • They found that hyperoxia occurred in almost one-fifth of patients, that patients with hyperoxia had greater in-hospital mortality than patients with normoxia or hypoxia and that, after controlling for some confounders, hyperoxia carried a clear independent association with mortality (odds ratio (OR), 1.8). (biomedcentral.com)
  • Their conclusion that hyperoxia is a robust predictor of mortality in patients after resuscitation form cardiac arrest was therefore potentially affected by selection bias and by insufficient adjustment for major confounders. (biomedcentral.com)
  • Compared with normoxia, hyperoxia was associated with higher mortality in overall patients (OR 1.22, 95% CI 1.12~1.33), as well as in the subgroups of cardiac arrest (OR 1.30, 95% CI 1.08~1.57) and extracorporeal life support (ELS) (OR 1.44, 95% CI 1.03~2.02). (biomedcentral.com)
  • Hyperoxia would lead to higher mortality in critically ill patients especially in the patients with cardiac arrest and ELS. (biomedcentral.com)
  • However, clinical studies testing the relationship between hyperoxia and mortality in critically ill patients have yielded conflicting results. (biomedcentral.com)
  • found a reduced mortality by hyperoxia while a contrary result was showed by Davis et al. (biomedcentral.com)
  • Although previous studies have performed the analysis of the relationship between hyperoxia and mortality, no solid conclusion has been drawn. (biomedcentral.com)
  • One showed no benefit, one showed a lower survival in non-hypoxic patients and one showed excess mortality in the hyperoxia group (2). (wikidot.com)
  • Next we determined the cardiopulmonary effects of PD123319 (0.1 mg·kg(-1)·day(-1)) in two models: early treatment during continuous exposure to hyperoxia for 10 days and late treatment starting on day 6 in rat pups exposed postnatally to hyperoxia for 9 days, followed by a 9-day recovery period in room air. (sigmaaldrich.com)
  • Systemic administration of the HIF-1α stabilizer dimethyloxalylglycine (DMOG) resulted in enhanced expression of HIF-1α and improved nephrogenesis: kidneys from hyperoxia-exposed pups treated with DMOG exhibited a nephrogenic zone width and glomerular diameter similar to room-air controls. (monash.edu)
  • In line with these clinical data are observations that hyperoxia in rat pups leads to increased endothelilal nitric oxide synthase (eNOS) levels, nitric oxide (NO) activity, hyperemia [ 7 , 8 ], and possibly eNOS uncoupling eventually leading to BPD. (biomedcentral.com)
  • Results showed that IL‑17D expression in intestine epithelial cells increased steadily, reaching a peak on day 7, and decreased gradually on days 10 and 14 under hyperoxia. (spandidos-publications.com)
  • In conclusion, the expression levels of intestinal IL‑17D and Nrf2 were altered simultaneously following neonatal rat development in hyperoxia, indicating that Nrf2 may be involved in regulating the expression of IL‑17D in intestinal epithelial cells. (spandidos-publications.com)
  • Moreover, IL‑17D in intestinal epithelial cells may play a unique immunological role during hyperoxia. (spandidos-publications.com)
  • Actually, inducible expression of KGF in mice exposed to hyperoxia protected the lung epithelium, but not the endothelium, from cell death, which is in keeping with the selective expression of KGF receptors on epithelial cells and not on endothelial cells ( 43 ). (physiology.org)
  • Hyperoxia provokes lung injury by inducing a primary massive necrosis of capillary endothelial cells and hence the loss of capillaries [ 7 - 9 ], which is followed by apoptosis/necrosis of the epithelial cells. (biomedcentral.com)
  • Overall, hyperoxia enhanced TMZ toxicity in GBM cells by induction of apoptosis, possibly via MAPK-related pathways. (biomedsearch.com)
  • Maturation-dependent oligodendrocyte apoptosis caused by hyperoxia. (semanticscholar.org)
  • 17β-estradiol suppresses hyperoxia-induced apoptosis of oligodendrocytes through paired-immunoglobulin-like receptor B. (semanticscholar.org)
  • To investigate effects of puerarin on apoptosis of microvascular endothelial cell, expression of transforming growth factor-β and vascular endothelial growth factor in the brain of hyperoxia-exposed neonatal rats, and to explore the molecular mechanism of the protective effects of puerarin on brain. (alliedacademies.org)
  • Puerarin may inhibit apoptosis and maintain the integrity of cerebral microvascular endothelial cells by down-regulating TGF-β expression and up-regulating VEGF expression, so as to promote angiogenesis after hyperoxia injury. (alliedacademies.org)
  • We hypothesized that the addition of hyperoxia to large-V T ventilation would increase neutrophil infiltration by upregulation of the cytokine macrophage inflammatory protein-2 (MIP-2) and would increase apoptosis via the mitogen-activated protein kinase pathways. (biomedcentral.com)
  • We hypothesized that the addition of hyperoxia to large-V T ventilation would increase MIP-2 production, neutrophil infiltration, and apoptosis via the MAPK pathways. (biomedcentral.com)
  • A change in practice was instituted in January 2003 with the objective of avoiding hyperoxia in preterm infants with target O2 saturation (SpO2) at 93 to 85% (Period II). (nih.gov)
  • In this study, the effect of resveratrol on the lung injury was evaluated in hyperoxia-exposed rats of preterm birth. (greenmedinfo.com)
  • Lang YD, Hung CL, Wu TY, Wang LF, Chen CM (2010) The renin-angiotensin system mediates hyperoxia-induced collagen production in human lung fibroblasts. (springer.com)
  • The hyperoxia-associated microcirculatory dysregulation and impaired tissue oxygenation known to take place in the presence of a physiologic hemoglobin concentration are not encountered in hemodiluted subjects. (uni-muenchen.de)
  • Noting that monitoring oxygenation using pulse oximetry alone "gives little information on PaO 2 " during conditions of normoxia and hyperoxia, Dr. Jaap Jan Vos and colleagues sought to evaluate the correlation of ORi to PaO 2 during moderate hyperoxia. (news-medical.net)
  • The cerebrovascular effects of hyperoxia may, therefore, be regionally specific and cannot be explained by a deoxyhemoglobin dilution model accounting for plasma oxygenation without assuming altered neuronal activity or altered neurovascular coupling. (tu-darmstadt.de)
  • This study investigated modulations of stimulus induced hemodynamic responses in the macaque monkey brain under anesthesia and hyperoxia. (tu-darmstadt.de)
  • Hyperoxia in Pediatric Anesthesia: Time for Reconsideration? (asahq.org)
  • These results suggest that hyperoxia induces K + efflux through the P2X7 receptor, leading to inflammasome activation and secretion of proinflammatory cytokines. (jimmunol.org)
  • 1 During mechanical ventilation, hyperoxia is not uncommon in the emergency room and intensive care unit during the management of SAH. (bmj.com)
  • Newborn animals exposed to hyperoxia, mechanical ventilation, or airway lipopolysaccharide represent models reproducing the impaired alveolarization observed in premature infants with BPD ( 1 , 41 , 52 ). (physiology.org)
  • C57BL/6 mice were exposed to high-V T (30 ml/kg) mechanical ventilation with room air or hyperoxia for one to five hours. (biomedcentral.com)
  • It was hypothesized that long-duration exposures to toxic levels of hyperoxia would have effects on respiratory control function or activity. (ingentaconnect.com)
  • We hypothesized that infusion of Vitamin C would abolish the effects of hyperoxia on the forearm blood flow (FBF) responses to exercise. (biomedsearch.com)
  • Based on the protective effects of hyperoxia that have already been demonstrated in animals, treating RD with supplemental O 2 may be a safe, relatively easy way to improve visual recovery during and after reattachment surgery. (arvojournals.org)
  • Therefore, we investigated the cardiopulmonary effects of BMP9 in neonatal Wistar rats with hyperoxia-induced BPD. (frontiersin.org)
  • Hyperoxia increased BM NO and circulating EPCs, effects inhibited by the NOS inhibitor N-nitro-l-arginine-methyl ester. (jci.org)
  • Collectively, these data suggest that the use of miR-184-3p specific inhibitors may act as novel therapeutic interventions to control the adverse effects of hyperoxia on lung development and function. (ersjournals.com)
  • Effects of progesterone on hyperoxia-induced damage in mouse C8-D1A astrocytes. (semanticscholar.org)
  • To this end, the effects of acute and chronichyperoxia exposure on metabolic rate and cardiorespiratory function (heart rate and ventilation rate) in Atlanticsalmon (Salmo salar) alevins incubated at 4 °C were investigated, and how it is affected by an increase in ambienttemperature (4 °C and 8 °C). Hyperoxia (15-18 days at 28 kPa) reared alevins display advanced development compared with normoxiaincubated animals. (edu.au)
  • The effects of hyperoxia on the lung have long been recognized. (biomedcentral.com)
  • Therefore, the aim of this study was to determine the effects of transient neonatal hyperoxia exposure on nephrogenesis. (monash.edu)
  • Here, we analyzed short- and long-term effects of neonatal hyperoxia on NOS3 and STAT3 expression and corresponding epigenetic signatures using a hyperoxia-based mouse model of BPD. (biomedcentral.com)
  • Administration of exogenous surfactant could have protective effects during hyperoxia. (springeropen.com)
  • Reference for Effects of hyperoxia on neutrophil adhesion. (woundreference.com)
  • We seek to: 1) assess whether low levels of positive pressure breathing can prevent atelectasis formation in humans during exposure to hyperoxia and +Gz-accelerations. (clinicaltrials.gov)
  • Systemic hyperoxia constricts the retinal arterioles and decreases the RBF in humans and animals through release of endothelin (ET)-1. (arvojournals.org)
  • Vitamin D seems to protect against hyperoxia-induced lung injury in newborn rats. (greenmedinfo.com)
  • We first investigated the role of AT2 inhibition with PD123319 (0.5 and 2 mg·kg(-1)·day(-1)) on the beneficial effect of AT2 agonist LP2-3 (5 μg/kg twice a day) on RVH in newborn rats with hyperoxia-induced BPD. (sigmaaldrich.com)
  • Mast cells mediate hyperoxia-induced airway hyperreactivity in newborn rats. (pubfacts.com)
  • This study combines two well-known vascular research models, hyperoxia and hind limb ischemia, aiming to better characterize capacities of the hyperoxia challenge. (inserm.fr)
  • These findings confirm the discriminative capacities of the hyperoxia challenge and suggest its potential utility to study other pathologies with vascular impact. (inserm.fr)
  • Early hyperoxia induced permanent changes in histones signatures at the NOS3 and STAT3 gene locus might partly explain the altered vascular response patterns in children with BPD. (biomedcentral.com)
  • Intratracheal treatment with exogenous surfactant protein B improved survival and lung histology in Stat-3-deleted mice during hyperoxia. (jci.org)
  • Subjects were studied at four levels of hyperoxia induced during a single session while perfusion was measured using arterial spin labelling MRI. (ox.ac.uk)
  • Because early, but not late, exposure resulted in compromised lung and cardiovascular development, we conclude that the consequences of hyperoxia are developmentally regulated and decrease with age. (luriechildrens.org)
  • We examined the independent relationship between hyperoxia and outcomes in such patients. (biomedcentral.com)
  • To determine the rate and severity of short- and long-term morbidity in very low birth weight infants treated before and after the implementation of a change in clinical practice designed to avoid hyperoxia. (nih.gov)
  • Hyperoxia may have a role in the clinical management of RD. Retinal reattachment surgery is frequently needed once a detachment is detected, but patients often must wait for a period before reattachment surgery. (arvojournals.org)
  • 6 , 7 Moreover, some clinical studies have reported that the hyperoxia-induced vasoconstriction in the retina deteriorates in patients with these diseases. (arvojournals.org)
  • Inga Karu, Peeter Tahepold, Arno Ruusalepp and Joel Starkopf, " Pretreatment by Hyperoxia - A Tool to Reduce Ischaemia-Reperfusion Injury in the Myocardium", Current Clinical Pharmacology (2010) 5: 125. (eurekaselect.com)
  • METHODS: Macrophage regulatory cytokine Colony-Stimulating Factor-1 (CSF-1) was investigated in a model of neonatal hyperoxia exposure, with the aim of promoting macrophages associated with alveologenesis to protect/rescue lung development and function. (monash.edu)
  • Our results showed that hyperoxia increased K + efflux, inflammasome formation, release of proinflammatory cytokines, and induction of caspase-1 and IL-1β cleavage both in vitro and in vivo. (jimmunol.org)
  • Furthermore, short hairpin RNA silencing of inflammasome components abrogated hyperoxia-induced secretion of proinflammatory cytokines in vitro. (jimmunol.org)
  • 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. (brightsurf.com)
  • These findings collectively indicate that BRP-39 is involved in repressing the M1 proinflammatory phenotype in hyperoxia, thereby deactivating inflammatory responses in macrophages and preventing neonatal lung injury. (hindawi.com)
  • Hyperoxia increased the average inner retinal P o 2 ( P IR ) in the detached retina to a level higher than that during normoxia. (arvojournals.org)
  • Hyperoxia has been shown to improve photoreceptor survival in the detached retina. (arvojournals.org)
  • Lin YJ, Markham NE, Balasubramaniam V et al (2005) Inhaled nitric oxide enhances distal lung growth after exposure to hyperoxia in neonatal rats. (springer.com)
  • Hyperoxia exposure leads to the development of lung injury and bronchial hyperreactivity (BHR) via involvement of nitric oxide (NO) pathway. (biomedcentral.com)
  • Administration of exogenous SDF-1alpha into wounds reversed the EPC homing impairment and, with hyperoxia, synergistically enhanced EPC mobilization, homing, neovascularization, and wound healing. (nih.gov)
  • A greater presence of myofibroblasts in LFs isolated from rats exposed to hyperoxia compared with those exposed to normoxia. (springer.com)
  • Effect of Vitamin C on Hyperoxia Induced Vasoconstriction in Exercising Skeletal Muscle. (biomedsearch.com)
  • 10 - 14 Previously, we also reported that ET-1 plays a major role in hyperoxia-induced vasoconstriction in cats. (arvojournals.org)
  • Hyperoxia can cause vasoconstriction of the carotid and downstream cerebral arteries. (wikidot.com)
  • While acute hypoxia generally leads to metabolic depression (≈70%, 21 kPa compared with5 kPa), acute hyperoxia (28 kPa) causes hypermetabolism (≈30% compared with normoxia at 4 °C and ≈20% at8 °C). Chronic hyperoxic rearing on the other hand did not alter metabolic rate at 4 °C or 8 °C in acute hyperoxia,normoxia or hypoxia. (edu.au)
  • however, the mechanisms connecting hyperoxia and the inflammatory response to lung damage is not clear. (jimmunol.org)