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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Hyperoxia is a medical term that refers to an abnormally high concentration of oxygen in the body or in a specific organ or tissue. It is often defined as the partial pressure of oxygen (PaO2) in arterial blood being greater than 100 mmHg.

This condition can occur due to various reasons such as exposure to high concentrations of oxygen during medical treatments, like mechanical ventilation, or due to certain diseases and conditions that cause the body to produce too much oxygen.

While oxygen is essential for human life, excessive levels can be harmful and lead to oxidative stress, which can damage cells and tissues. Hyperoxia has been linked to various complications, including lung injury, retinopathy of prematurity, and impaired wound healing.

Oxygen is a colorless, odorless, tasteless gas that constitutes about 21% of the earth's atmosphere. It is a crucial element for human and most living organisms as it is vital for respiration. Inhaled oxygen enters the lungs and binds to hemoglobin in red blood cells, which carries it to tissues throughout the body where it is used to convert nutrients into energy and carbon dioxide, a waste product that is exhaled.

Medically, supplemental oxygen therapy may be provided to patients with conditions such as chronic obstructive pulmonary disease (COPD), pneumonia, heart failure, or other medical conditions that impair the body's ability to extract sufficient oxygen from the air. Oxygen can be administered through various devices, including nasal cannulas, face masks, and ventilators.

Pulmonary alveoli, also known as air sacs, are tiny clusters of air-filled pouches located at the end of the bronchioles in the lungs. They play a crucial role in the process of gas exchange during respiration. The thin walls of the alveoli, called alveolar membranes, allow oxygen from inhaled air to pass into the bloodstream and carbon dioxide from the bloodstream to pass into the alveoli to be exhaled out of the body. This vital function enables the lungs to supply oxygen-rich blood to the rest of the body and remove waste products like carbon dioxide.

Hyperbaric oxygenation is a medical treatment in which a patient breathes pure oxygen in a pressurized chamber, typically at greater than one atmosphere absolute (ATA). This process results in increased levels of oxygen being dissolved in the blood and delivered to body tissues, thereby promoting healing, reducing inflammation, and combating infection. Hyperbaric oxygen therapy is used to treat various medical conditions, including carbon monoxide poisoning, decompression sickness, gangrene, and wounds that are slow to heal due to diabetes or radiation injury.

A lung is a pair of spongy, elastic organs in the chest that work together to enable breathing. They are responsible for taking in oxygen and expelling carbon dioxide through the process of respiration. The left lung has two lobes, while the right lung has three lobes. The lungs are protected by the ribcage and are covered by a double-layered membrane called the pleura. The trachea divides into two bronchi, which further divide into smaller bronchioles, leading to millions of tiny air sacs called alveoli, where the exchange of gases occurs.

"Newborn animals" refers to the very young offspring of animals that have recently been born. In medical terminology, newborns are often referred to as "neonates," and they are classified as such from birth until about 28 days of age. During this time period, newborn animals are particularly vulnerable and require close monitoring and care to ensure their survival and healthy development.

The specific needs of newborn animals can vary widely depending on the species, but generally, they require warmth, nutrition, hydration, and protection from harm. In many cases, newborns are unable to regulate their own body temperature or feed themselves, so they rely heavily on their mothers for care and support.

In medical settings, newborn animals may be examined and treated by veterinarians to ensure that they are healthy and receiving the care they need. This can include providing medical interventions such as feeding tubes, antibiotics, or other treatments as needed to address any health issues that arise. Overall, the care and support of newborn animals is an important aspect of animal medicine and conservation efforts.

Anoxia is a medical condition that refers to the absence or complete lack of oxygen supply in the body or a specific organ, tissue, or cell. This can lead to serious health consequences, including damage or death of cells and tissues, due to the vital role that oxygen plays in supporting cellular metabolism and energy production.

Anoxia can occur due to various reasons, such as respiratory failure, cardiac arrest, severe blood loss, carbon monoxide poisoning, or high altitude exposure. Prolonged anoxia can result in hypoxic-ischemic encephalopathy, a serious condition that can cause brain damage and long-term neurological impairments.

Medical professionals use various diagnostic tests, such as blood gas analysis, pulse oximetry, and electroencephalography (EEG), to assess oxygen levels in the body and diagnose anoxia. Treatment for anoxia typically involves addressing the underlying cause, providing supplemental oxygen, and supporting vital functions, such as breathing and circulation, to prevent further damage.

The carotid body is a small chemoreceptor organ located near the bifurcation of the common carotid artery into the internal and external carotid arteries. It plays a crucial role in the regulation of respiration, blood pressure, and pH balance by detecting changes in the chemical composition of the blood, particularly oxygen levels, carbon dioxide levels, and hydrogen ion concentration (pH).

The carotid body contains specialized nerve endings called glomus cells that are sensitive to changes in these chemical parameters. When there is a decrease in oxygen or an increase in carbon dioxide or hydrogen ions, the glomus cells release neurotransmitters such as acetylcholine and dopamine, which activate afferent nerve fibers leading to the brainstem's nucleus tractus solitarius. This information is then integrated with other physiological signals in the brainstem, resulting in appropriate adjustments in breathing rate, depth, and pattern, as well as changes in heart rate and blood vessel diameter to maintain homeostasis.

Dysfunction of the carotid body can lead to various disorders, such as hypertension, sleep apnea, and chronic lung disease. In some cases, overactivity of the carotid body may result in conditions like primary breathing pattern disorders or pseudohypoxia, where the body responds as if it is experiencing hypoxia despite normal oxygen levels.

In the context of medicine, and specifically in physiology and respiratory therapy, partial pressure (P or p) is a measure of the pressure exerted by an individual gas in a mixture of gases. It's commonly used to describe the concentrations of gases in the body, such as oxygen (PO2), carbon dioxide (PCO2), and nitrogen (PN2).

The partial pressure of a specific gas is calculated as the fraction of that gas in the total mixture multiplied by the total pressure of the mixture. This concept is based on Dalton's law, which states that the total pressure exerted by a mixture of gases is equal to the sum of the pressures exerted by each individual gas.

For example, in room air at sea level, the partial pressure of oxygen (PO2) is approximately 160 mmHg (mm of mercury), which represents about 21% of the total barometric pressure (760 mmHg). This concept is crucial for understanding gas exchange in the lungs and how gases move across membranes, such as from alveoli to blood and vice versa.

Chemoreceptor cells are specialized sensory neurons that detect and respond to chemical changes in the internal or external environment. They play a crucial role in maintaining homeostasis within the body by converting chemical signals into electrical impulses, which are then transmitted to the central nervous system for further processing and response.

There are two main types of chemoreceptor cells:

1. Oxygen Chemoreceptors: These cells are located in the carotid bodies near the bifurcation of the common carotid artery and in the aortic bodies close to the aortic arch. They monitor the levels of oxygen, carbon dioxide, and pH in the blood and respond to decreases in oxygen concentration or increases in carbon dioxide and hydrogen ions (indicating acidity) by increasing their firing rate. This signals the brain to increase respiratory rate and depth, thereby restoring normal oxygen levels.

2. Taste Cells: These chemoreceptor cells are found within the taste buds of the tongue and other areas of the oral cavity. They detect specific tastes (salty, sour, sweet, bitter, and umami) by interacting with molecules from food. When a tastant binds to receptors on the surface of a taste cell, it triggers a series of intracellular signaling events that ultimately lead to the generation of an action potential. This information is then relayed to the brain, where it is interpreted as taste sensation.

In summary, chemoreceptor cells are essential for maintaining physiological balance by detecting and responding to chemical stimuli in the body. They play a critical role in regulating vital functions such as respiration and digestion.

Lung injury, also known as pulmonary injury, refers to damage or harm caused to the lung tissue, blood vessels, or air sacs (alveoli) in the lungs. This can result from various causes such as infection, trauma, exposure to harmful substances, or systemic diseases. Common types of lung injuries include acute respiratory distress syndrome (ARDS), pneumonia, and chemical pneumonitis. Symptoms may include difficulty breathing, cough, chest pain, and decreased oxygen levels in the blood. Treatment depends on the underlying cause and may include medications, oxygen therapy, or mechanical ventilation.

Ion-Selective Electrodes (ISEs) are a type of chemical sensor that measure the activity of specific ions in a solution. They work by converting the chemical response into an electrical signal, which can then be measured and analyzed. The electrode is coated with a membrane that is selectively permeable to a particular ion, allowing for the detection and measurement of that specific ion in the presence of other ions.

ISEs are widely used in various fields such as clinical chemistry, biomedical research, environmental monitoring, and industrial process control. In medical diagnostics, ISEs are commonly used to measure the levels of ions such as sodium, potassium, chloride, and calcium in biological samples like blood, urine, and cerebrospinal fluid.

The response of an ISE is based on Nernst's equation, which relates the electrical potential across the membrane to the activity of the ion being measured. The selectivity of the electrode for a particular ion is determined by the type of membrane used, and the choice of membrane depends on the application and the specific ions to be measured.

Overall, Ion-Selective Electrodes are important tools in medical diagnostics and research, providing accurate and reliable measurements of ion activity in biological systems.

Retinal vessels refer to the blood vessels that are located in the retina, which is the light-sensitive tissue that lines the inner surface of the eye. The retina contains two types of blood vessels: arteries and veins.

The central retinal artery supplies oxygenated blood to the inner layers of the retina, while the central retinal vein drains deoxygenated blood from the retina. These vessels can be visualized during a routine eye examination using an ophthalmoscope, which allows healthcare professionals to assess their health and any potential abnormalities.

Retinal vessels are essential for maintaining the health and function of the retina, and any damage or changes to these vessels can affect vision and lead to various eye conditions such as diabetic retinopathy, retinal vein occlusion, and hypertensive retinopathy.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease that primarily affects premature infants. It is defined as the need for supplemental oxygen at 28 days of life or beyond, due to abnormal development and injury to the lungs.

The condition was first described in the 1960s, following the introduction of mechanical ventilation and high concentrations of oxygen therapy for premature infants with respiratory distress syndrome (RDS). These treatments, while lifesaving, can also cause damage to the delicate lung tissue, leading to BPD.

The pathogenesis of BPD is complex and involves an interplay between genetic factors, prenatal exposures, and postnatal injury from mechanical ventilation and oxygen toxicity. Inflammation, oxidative stress, and impaired lung development contribute to the development of BPD.

Infants with BPD typically have abnormalities in their airways, alveoli (air sacs), and blood vessels in the lungs. These changes can lead to symptoms such as difficulty breathing, wheezing, coughing, and poor growth. Treatment may include oxygen therapy, bronchodilators, corticosteroids, diuretics, and other medications to support lung function and minimize complications.

The prognosis for infants with BPD varies depending on the severity of the disease and associated medical conditions. While some infants recover completely, others may have long-term respiratory problems that require ongoing management.

Retinopathy of Prematurity (ROP) is a potentially sight-threatening proliferative retinal vascular disorder that primarily affects prematurely born infants, particularly those with low birth weight and/or young gestational age. It is characterized by the abnormal growth and development of retinal blood vessels due to disturbances in the oxygen supply and metabolic demands during critical phases of fetal development.

The condition can be classified into various stages (1-5) based on its severity, with stages 4 and 5 being more severe forms that may lead to retinal detachment and blindness if left untreated. The pathogenesis of ROP involves an initial phase of vessel loss and regression in the central retina, followed by a secondary phase of abnormal neovascularization, which can cause fibrosis, traction, and ultimately, retinal detachment.

ROP is typically managed with a multidisciplinary approach involving ophthalmologists, neonatologists, and pediatricians. Treatment options include laser photocoagulation, cryotherapy, intravitreal anti-VEGF injections, or even surgical interventions to prevent retinal detachment and preserve vision. Regular screening examinations are crucial for early detection and timely management of ROP in at-risk infants.

Pneumocytes are specialized epithelial cells that line the alveoli, which are the tiny air sacs in the lungs where gas exchange occurs. There are two main types of pneumocytes: type I and type II.

Type I pneumocytes are flat, thin cells that cover about 95% of the alveolar surface area. They play a crucial role in facilitating the diffusion of oxygen and carbon dioxide between the alveoli and the bloodstream. Type I pneumocytes also contribute to maintaining the structural integrity of the alveoli.

Type II pneumocytes are smaller, more cuboidal cells that produce and secrete surfactant, a substance composed of proteins and lipids that reduces surface tension within the alveoli, preventing their collapse and facilitating breathing. Type II pneumocytes can also function as progenitor cells, capable of differentiating into type I pneumocytes to help repair damaged lung tissue.

In summary, pneumocytes are essential for maintaining proper gas exchange in the lungs and contributing to the overall health and functioning of the respiratory system.

Electrochemical Scanning Microscopy (ESCM) is not a specific type of microscopy on its own, but rather refers to various techniques that combine scanning probe microscopy with electrochemistry. These techniques use a sharp probe to scan the surface of a sample while simultaneously measuring or applying an electrical potential. This allows for the visualization and manipulation of electrochemical processes at the nanoscale.

There are several types of ESCM, including:

1. Scanning Electrochemical Microscopy (SECM): A technique that measures the local electrochemical activity of a sample by scanning a microelectrode over its surface while monitoring changes in current. This can be used to map out the distribution of redox-active species, measure local pH or potential, and study corrosion processes.

2. Scanning Ion Conductance Microscopy (SICM): A technique that measures the ion conductance between a nanopipette and a sample surface to create topographic images with high resolution. SICM can be used to investigate biological samples, such as cells and tissues, in their native environment without causing damage.

3. Scanning Kelvin Probe Microscopy (SKPM): A technique that measures the contact potential difference between a conductive probe and a sample surface. This allows for the mapping of work function differences, which can provide information about chemical composition and electronic properties.

4. Piezoresponse Force Microscopy (PFM): A technique that uses an electric field to induce mechanical deformation in ferroelectric or piezoelectric materials. By monitoring these deformations, PFM can be used to map the local polarization and investigate nanoscale electromechanical properties.

5. Scanning Electrochemical Strain Microscopy (SESM): A technique that combines scanning probe microscopy with electrochemical strain measurements to study mechanical deformations in materials under an applied potential. SESM can be used to investigate the relationship between electrochemical processes and mechanical properties at the nanoscale.

In summary, Electrochemical Scanning Microscopy (ESCM) encompasses various techniques that combine scanning probe microscopy with electrochemical measurements or manipulations. These methods provide valuable insights into the structure, composition, and properties of materials at the nanoscale, enabling advancements in fields such as energy storage, electronics, biology, and materials science.

Carbon dioxide (CO2) is a colorless, odorless gas that is naturally present in the Earth's atmosphere. It is a normal byproduct of cellular respiration in humans, animals, and plants, and is also produced through the combustion of fossil fuels such as coal, oil, and natural gas.

In medical terms, carbon dioxide is often used as a respiratory stimulant and to maintain the pH balance of blood. It is also used during certain medical procedures, such as laparoscopic surgery, to insufflate (inflate) the abdominal cavity and create a working space for the surgeon.

Elevated levels of carbon dioxide in the body can lead to respiratory acidosis, a condition characterized by an increased concentration of carbon dioxide in the blood and a decrease in pH. This can occur in conditions such as chronic obstructive pulmonary disease (COPD), asthma, or other lung diseases that impair breathing and gas exchange. Symptoms of respiratory acidosis may include shortness of breath, confusion, headache, and in severe cases, coma or death.

Oxygen consumption, also known as oxygen uptake, is the amount of oxygen that is consumed or utilized by the body during a specific period of time, usually measured in liters per minute (L/min). It is a common measurement used in exercise physiology and critical care medicine to assess an individual's aerobic metabolism and overall health status.

In clinical settings, oxygen consumption is often measured during cardiopulmonary exercise testing (CPET) to evaluate cardiovascular function, pulmonary function, and exercise capacity in patients with various medical conditions such as heart failure, chronic obstructive pulmonary disease (COPD), and other respiratory or cardiac disorders.

During exercise, oxygen is consumed by the muscles to generate energy through a process called oxidative phosphorylation. The amount of oxygen consumed during exercise can provide important information about an individual's fitness level, exercise capacity, and overall health status. Additionally, measuring oxygen consumption can help healthcare providers assess the effectiveness of treatments and rehabilitation programs in patients with various medical conditions.

Blood gas analysis is a medical test that measures the levels of oxygen and carbon dioxide in the blood, as well as the pH level, which indicates the acidity or alkalinity of the blood. This test is often used to evaluate lung function, respiratory disorders, and acid-base balance in the body. It can also be used to monitor the effectiveness of treatments for conditions such as chronic obstructive pulmonary disease (COPD), asthma, and other respiratory illnesses. The analysis is typically performed on a sample of arterial blood, although venous blood may also be used in some cases.

Oxygen inhalation therapy is a medical treatment that involves the administration of oxygen to a patient through a nasal tube or mask, with the purpose of increasing oxygen concentration in the body. This therapy is used to treat various medical conditions such as chronic obstructive pulmonary disease (COPD), pneumonia, heart failure, and other conditions that cause low levels of oxygen in the blood. The additional oxygen helps to improve tissue oxygenation, reduce work of breathing, and promote overall patient comfort and well-being. Oxygen therapy may be delivered continuously or intermittently, depending on the patient's needs and medical condition.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Hypercapnia is a state of increased carbon dioxide (CO2) concentration in the blood, typically defined as an arterial CO2 tension (PaCO2) above 45 mmHg. It is often associated with conditions that impair gas exchange or eliminate CO2 from the body, such as chronic obstructive pulmonary disease (COPD), severe asthma, respiratory failure, or certain neuromuscular disorders. Hypercapnia can cause symptoms such as headache, confusion, shortness of breath, and in severe cases, it can lead to life-threatening complications such as respiratory acidosis, coma, and even death if not promptly treated.

Medical Definition of Respiration:

Respiration, in physiology, is the process by which an organism takes in oxygen and gives out carbon dioxide. It's also known as breathing. This process is essential for most forms of life because it provides the necessary oxygen for cellular respiration, where the cells convert biochemical energy from nutrients into adenosine triphosphate (ATP), and releases waste products, primarily carbon dioxide.

In humans and other mammals, respiration is a two-stage process:

1. Breathing (or external respiration): This involves the exchange of gases with the environment. Air enters the lungs through the mouth or nose, then passes through the pharynx, larynx, trachea, and bronchi, finally reaching the alveoli where the actual gas exchange occurs. Oxygen from the inhaled air diffuses into the blood, while carbon dioxide, a waste product of metabolism, diffuses from the blood into the alveoli to be exhaled.

2. Cellular respiration (or internal respiration): This is the process by which cells convert glucose and other nutrients into ATP, water, and carbon dioxide in the presence of oxygen. The carbon dioxide produced during this process then diffuses out of the cells and into the bloodstream to be exhaled during breathing.

In summary, respiration is a vital physiological function that enables organisms to obtain the necessary oxygen for cellular metabolism while eliminating waste products like carbon dioxide.

Respiratory mechanics refers to the biomechanical properties and processes that involve the movement of air through the respiratory system during breathing. It encompasses the mechanical behavior of the lungs, chest wall, and the muscles of respiration, including the diaphragm and intercostal muscles.

Respiratory mechanics includes several key components:

1. **Compliance**: The ability of the lungs and chest wall to expand and recoil during breathing. High compliance means that the structures can easily expand and recoil, while low compliance indicates greater resistance to expansion and recoil.
2. **Resistance**: The opposition to airflow within the respiratory system, primarily due to the friction between the air and the airway walls. Airway resistance is influenced by factors such as airway diameter, length, and the viscosity of the air.
3. **Lung volumes and capacities**: These are the amounts of air present in the lungs during different phases of the breathing cycle. They include tidal volume (the amount of air inspired or expired during normal breathing), inspiratory reserve volume (additional air that can be inspired beyond the tidal volume), expiratory reserve volume (additional air that can be exhaled beyond the tidal volume), and residual volume (the air remaining in the lungs after a forced maximum exhalation).
4. **Work of breathing**: The energy required to overcome the resistance and elastic forces during breathing. This work is primarily performed by the respiratory muscles, which contract to generate negative intrathoracic pressure and expand the chest wall, allowing air to flow into the lungs.
5. **Pressure-volume relationships**: These describe how changes in lung volume are associated with changes in pressure within the respiratory system. Important pressure components include alveolar pressure (the pressure inside the alveoli), pleural pressure (the pressure between the lungs and the chest wall), and transpulmonary pressure (the difference between alveolar and pleural pressures).

Understanding respiratory mechanics is crucial for diagnosing and managing various respiratory disorders, such as chronic obstructive pulmonary disease (COPD), asthma, and restrictive lung diseases.

In medical terms, 'air' is defined as the mixture of gases that make up the Earth's atmosphere. It primarily consists of nitrogen (78%), oxygen (21%), and small amounts of other gases such as argon, carbon dioxide, and trace amounts of neon, helium, and methane.

Air is essential for human life, as it provides the oxygen that our bodies need to produce energy through respiration. We inhale air into our lungs, where oxygen is absorbed into the bloodstream and transported to cells throughout the body. At the same time, carbon dioxide, a waste product of cellular metabolism, is exhaled out of the body through the lungs and back into the atmosphere.

In addition to its role in respiration, air also plays a critical role in regulating the Earth's climate and weather patterns, as well as serving as a medium for sound waves and other forms of energy transfer.

Pulmonary surfactant-associated protein C (SP-C) is a small hydrophobic protein that is a component of pulmonary surfactant. Surfactant is a complex mixture of lipids and proteins that reduces surface tension in the alveoli of the lungs, preventing collapse during expiration and facilitating lung expansion during inspiration. SP-C plays a crucial role in maintaining the structural integrity and stability of the surfactant film at the air-liquid interface of the alveoli.

Deficiency or dysfunction of SP-C has been associated with several pulmonary diseases, including respiratory distress syndrome (RDS) in premature infants, interstitial lung diseases (ILDs), and pulmonary fibrosis. Mutations in the gene encoding SP-C (SFTPC) can lead to abnormal protein processing and accumulation, resulting in lung injury and inflammation, ultimately contributing to the development of these conditions.

Hyperoxia is the opposite of hypoxia; hyperoxia refers to a state in which oxygen supply to the tissues is excessive, and ... Hyperoxia occurs when cells, tissues and organs are exposed to an excess supply of oxygen (O2) or higher than normal partial ... In the environment, hyperoxia refers to an abnormally high oxygen concentration in a body of water or other habitat. Associated ... The highest risk of hyperoxia is in hyperbaric oxygen therapy, where it is a high probability side effect of the treatment for ...
However, hyperoxia causes lung injury and pathological changes. Notably, preclinical data suggest that aspirin modulates ... This study demonstrated that aspirin exerts a protective effect for hyperoxia-induced lung injury and thus is currently the ... to investigate the mechanisms of aspirins anti-inflammatory and antioxidant effects on hyperoxia-induced ALI in nuclear factor ... neutrophil infiltration and lung edema compared with treatment with only hyperoxia treatment. In addition, we demonstrated that ...
Postnatal hyperoxia exposure in rodents is a well-established model of chronic lung disease of prematurity, and also ... Postnatal hyperoxia exposure in rodents is a well-established model of chronic lung disease of prematurity, and also ... Compared to control rats, male rats exposed to 14 days of postnatal hyperoxia then aged to 1 year demonstrated higher skeletal ... Compared to control rats, male rats exposed to 14 days of postnatal hyperoxia then aged to one year demonstrated higher ...
Effect of hyperoxia and hypoxia on exercise-induced breathlessness in normal subjects N. Chronos; N. Chronos ... N. Chronos, L. Adams, A. Guz; Effect of hyperoxia and hypoxia on exercise-induced breathlessness in normal subjects. Clin Sci ( ...
NOS and COX isoforms and abnormal microvessel responses to CO2 and H+ in hyperoxia-injured lungs. K. Naoki, H. Kudo, K. Suzuki ... Differential effects of hyperoxia on the inducible and constitutive isoforms of nitric oxide synthase in the lung. Shock 1997;7 ... 3⇓). These results suggest that iNOS expression is not enhanced in lungs exposed to hyperoxia for 48 h. These findings are ... ecNOS and COX‐1, but not iNOS and COX‐2, were upregulated in hyperoxia-injured lungs. The nitric oxide produced by ecNOS ...
Intravitreal administration of recombinant human opticin protects against hyperoxia-induced pre-retinal neovascularization. ... Intravitreal administration of recombinant human opticin protects against hyperoxia-induced pre-retinal neovascularization ... Intravitreal administration of recombinant human opticin protects against hyperoxia-induced pre-retinal neovascularization. ...
Short-duration hyperoxia causes genotoxicity in mouse lungs: protection by volatile anesthetic isoflurane. Am J Physiol Lung ... "Hyperoxia" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1a Signaling and Limits Oxygen Toxicity. Am J Respir Cell ... This graph shows the total number of publications written about "Hyperoxia" by people in UAMS Profiles by year, and whether " ...
3GF-MIXER-HYPEROXIA. 3GF Mixer-Hypoxia is a 3 gas mixer (Carbon Dioxide, Oxygen, Nitrogen) which employs floating ball ...
Bibliographic details on Characterization of cerebrovascular responses to hyperoxia and hypercapnia using MRI in rat. ... Characterization of cerebrovascular responses to hyperoxia and hypercapnia using MRI in rat. NeuroImage 45(4): 1126-1134 (2009) ...
Hyperoxia increases the uptake of 5-fluorouracil in mammary tumors independently of changes in interstitial fluid pressure and ... The aim of this study was to elucidate whether hyperoxia also enhances any actual uptake of 5FU (5-fluorouracil)… ...
The Neonatal Neurodevelopmental Follow-Up Clinic sees approximately 350 high risk patients from the NICU and the Cardiac Critical Care Unit. Children are followed to three years of age by an interdisciplinary team with expertise in neurodevelopmental assessment and therapy. There are combined clinics with Neurology to optimize coordination of care ...
Hyperoxia: Too much of a good thing. July 6th, 2020 CapnoAcademy Articles, Learn ... Normobaric hyperoxia reduces cardiac index in patients after coronary artery bypass surgery. J Cardiothorac Vasc Anesth 2005;19 ... Here are essential points to remember about hyperoxia:. *There are three significant consequences of routine, excessive oxygen ... However, consider these three points of evidence: One study showed that hyperoxia reduced cardiac output by 10-15% in both ...
2010_Binda-2010-Hyperoxia-and-prevention-of-adhesio. by Philippe Koninckx , Aug 29, 2020 ...
Diagnosis if a Baby is Blue and Hyperoxia Test & boost your knowledge! Study for your classes, USMLE, MCAT or MBBS. Learn ... Which of the following congenital heart diseases is most likely the cause of PaO₂ < 40 mm Hg after a hyperoxia test in an ... Author of lecture Diagnosis if a Baby is Blue and Hyperoxia Test Brian Alverson, MD. ... The lecture Diagnosis if a Baby is Blue and Hyperoxia Test by Brian Alverson, MD is from the course Pediatric Cardiology. ...
Neonatal Sprague Dawley rats were reared in either room air (RA) or hyperoxia (85% O2) from postnatal days 1 to 14. On ... The rats reared in hyperoxia and treated with NS yielded significantly higher mean linear intercepts (MLIs) and interleukin (IL ... Our previous study found that mesenchymal stem cells (MSCs) attenuated hyperoxia-induced lung injury and the combination ... Consecutive daily administration of intratracheal surfactant and hUC-MSCs can be an effective regimen for treating hyperoxia- ...
Hyperoxia was associated with a small net gain of Na+ and large net losses of Cl- at the gills, while normoxic recovery was ... Hyperoxia was associated with a small net gain of Na+ and large net losses of Cl- at the gills, while normoxic recovery was ... Hyperoxia was associated with a small net gain of Na+ and large net losses of Cl- at the gills, while normoxic recovery was ... Hyperoxia was associated with a small net gain of Na+ and large net losses of Cl- at the gills, while normoxic recovery was ...
Normobaric hyperoxia (NBHO) is both a non-invasive and easy method that seems to be able to improve outcomes after cerebral ...
Background/aim: Hyperoxia- and inflammation-induced lung injury is an important cause of the development of bronchopulmonary ... We aimed to ascertain the beneficial effects of ginger (Zingiber officinale) on rat pups exposed to hyperoxia and inflammation ... Ginger (Zingiber officinale) prevents severe damage to the lungs due to hyperoxia and inflammation ...
"Inhaled ethyl nitrite prevents hyperoxia-impaired postnatal alveolar development in newborn rats." Am J Respir Crit Care Med ... "Inhaled ethyl nitrite prevents hyperoxia-impaired postnatal alveolar development in newborn rats." Am J Respir Crit Care Med, ... Inhaled ethyl nitrite prevents hyperoxia-impaired postnatal alveolar development in newborn rats.. Publication , Journal ... ENO prevented hyperoxia impairments of lung compliance and postnatal alveolar development in newborn rats. ...
Hyperoxia for an average of 17 hours did not change the total number or type of lung inflammatory and immune effector cells ... Hyperoxia for an average of 17 hours did not change the total number or type of lung inflammatory and immune effector cells ... Hyperoxia for an average of 17 hours did not change the total number or type of lung inflammatory and immune effector cells ... Hyperoxia for an average of 17 hours did not change the total number or type of lung inflammatory and immune effector cells ...
... the long-term pulmonary consequences of neonatal hyperoxia are unknown. Here, we investigate whether neonatal hyperoxia alters ... the long-term pulmonary consequences of neonatal hyperoxia are unknown. Here, we investigate whether neonatal hyperoxia alters ... the long-term pulmonary consequences of neonatal hyperoxia are unknown. Here, we investigate whether neonatal hyperoxia alters ... the long-term pulmonary consequences of neonatal hyperoxia are unknown. Here, we investigate whether neonatal hyperoxia alters ...
Which of the below statements is TRUE regarding hyperoxia (excessive oxygen) in the ED?. ... Comments Off on Which of the below statements is TRUE regarding hyperoxia (excessive oxygen) in the ED? ...
ContextLaboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic ... Results Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group ... Hyperoxia was defined as PaO2 of 300 mm Hg or greater8; hypoxia, PaO2 of less than 60 mm Hg (or ratio of PaO2 to fraction of ... Hyperoxia was defined as PaO2 of 300 mm Hg or greater; hypoxia, PaO2 of less than 60 mm Hg (or ratio of PaO2 to fraction of ...
Gershenovich Z.S., Krichevskaia A.A., Shugaleĭ V.S., Andreev M.L. (1972) Protective effect of urea in hyperoxia. Content of ... Gershenovich Z.S. et al., Protective effect of urea in hyperoxia. Content of free and bound forms of urea in the brain. ... Protective effect of urea in hyperoxia. Content of free and bound forms of urea in the brain // Voprosy Meditsinskoi Khimii. - ... Gershenovich, Z. S., Krichevskaia, A. A., Shugaleĭ, V. S., Andreev, M. L. (1972). Protective effect of urea in hyperoxia. ...
Hypoxia and hyperoxia treatments. To test the hypothesis that A. socius embryos experience tissue hypoxia early in development ... Embryos exposed to hyperoxia (40% O2) exhibit a significant 37%decrease in [AMP]:[ATP] compared with control embryos (ANOVA F= ... Embryos incubated for 24 h under normoxia (20% O2), hyperoxia (40% O2), or mild hypoxia (10% O2) did not exhibit any ... hyperoxia (air supplemented with pure O2, final concentration 40%) or mild hypoxia (air mixed with N2, final O2 concentration ...
Cathelicidin attenuates hyperoxia-induced intestinal injury through inhibition of NF-κB activity in newborn rats. / Chou, Hsiu ... Cathelicidin attenuates hyperoxia-induced intestinal injury through inhibition of NF-κB activity in newborn rats. Experimental ... Cathelicidin attenuates hyperoxia-induced intestinal injury through inhibition of NF-κB activity in newborn rats. In: ... Sprague-Dawley rat pups were reared in either room air (RA) or hyperoxia (85% O2) and were randomly treated with low-dose ...

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