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Claude A Piantadosi - One of the best experts on this subject based on the ideXlab platform.
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adrenoceptor blockade modifies regional cerebral blood flow responses to hyperbaric hyperoxia protection against cns Oxygen Toxicity
Journal of Applied Physiology, 2018Co-Authors: Heath G Gasier, Ivan T Demchenko, Sergei Yu Zhilyaev, A N Moskvin, A I Krivchenko, Claude A PiantadosiAbstract:Blocking adrenergic receptors with phentolamine (nonselective α1 and α2), prazosin (selective α1), propranolol (nonselective β1 and β2), and atenolol (selective β1) modified cardiovascular and regi...
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Oxygen Toxicity from cough to convulsion
2015Co-Authors: Marlon A Medford, Claude A PiantadosiAbstract:Oxygen is by its chemical nature a toxic molecule and organisms that survive in its presence have evolved potent antioxidant defenses. Through basic and clinical research we have come to understand many of the mechanisms of Oxygen (O2) Toxicity as well as measures that mitigate its risks. When the partial pressure of Oxygen (PO2) is increased in the cell, the formation of reactive Oxygen species (ROS) is enhanced at multiple locations, such as in the mitochondria. ROS attack biological macromolecules, which disrupts homeostasis and causes tissue and organ system dysfunction that will ultimately be lethal. An Oxygen partial pressure (PO2) of 0.21 to 1.0 atm absolute (ATA) is in the normobaric range while a PO2 above 1.0 ATA is termed hyperbaric hyperoxia. As the PO2 in the normobaric range increases, specific physiological disturbances, such as disordered pulmonary gas exchange and retinopathy of prematurity appear, while others occur exclusively at hyperbaric pressures such as peripheral visual loss, seizures, and neurogenic pulmonary injury. Ultimately, the utility of O2 is limited by this Toxicity and its therapeutic applications in medicine, aeronautics, and diving must be counterbalanced by the risk of harm.
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two faces of nitric oxide implications for cellular mechanisms of Oxygen Toxicity
Journal of Applied Physiology, 2009Co-Authors: Barry W Allen, I T Demchenko, Claude A PiantadosiAbstract:Recent investigations have elucidated some of the diverse roles played by reactive Oxygen and nitrogen species in events that lead to Oxygen Toxicity and defend against it. The focus of this review is on toxic and protective mechanisms in hyperoxia that have been investigated in our laboratories, with an emphasis on interactions of nitric oxide (NO) with other endogenous chemical species and with different physiological systems. It is now emerging from these studies that the anatomical localization of NO release, which depends, in part, on whether the Oxygen exposure is normobaric or hyperbaric, strongly influences whether Toxicity emerges and what form it takes, for example, acute lung injury, central nervous system excitation, or both. Spatial effects also contribute to differences in the susceptibility of different cells in organs at risk from hyperoxia, especially in the brain and lungs. As additional nodes are identified in this interactive network of toxic and protective responses, future advances may open up the possibility of novel pharmacological interventions to extend both the time and partial pressures of Oxygen exposures that can be safely tolerated. The implications of a better understanding of the mechanisms by which NO contributes to central nervous system Oxygen Toxicity may include new insights into the pathogenesis of seizures of diverse etiologies. Likewise, improved knowledge of NO-based mechanisms of pulmonary Oxygen Toxicity may enhance our understanding of other types of lung injury associated with oxidative or nitrosative stress.
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contributions of nitric oxide synthase isoforms to pulmonary Oxygen Toxicity local vs mediated effects
American Journal of Physiology-lung Cellular and Molecular Physiology, 2008Co-Authors: I T Demchenko, Claude A Piantadosi, Dmitriy N Atochin, Diana Gutsaeva, Ryan R Godfrey, Paul L Huang, Barry W AllenAbstract:Reactive species of Oxygen and nitrogen have been collectively implicated in pulmonary Oxygen Toxicity, but the contributions of specific molecules are unknown. Therefore, we assessed the roles of ...
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similar but not the same normobaric and hyperbaric pulmonary Oxygen Toxicity the role of nitric oxide
American Journal of Physiology-lung Cellular and Molecular Physiology, 2007Co-Authors: I T Demchenko, Barry W Allen, Karen E Weltywolf, Claude A PiantadosiAbstract:Pulmonary manifestations of Oxygen Toxicity were studied and quantified in rats breathing >98% O2 at 1, 1.5, 2, 2.5, and 3 ATA to test our hypothesis that different patterns of pulmonary injury wou...
I T Demchenko - One of the best experts on this subject based on the ideXlab platform.
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two faces of nitric oxide implications for cellular mechanisms of Oxygen Toxicity
Journal of Applied Physiology, 2009Co-Authors: Barry W Allen, I T Demchenko, Claude A PiantadosiAbstract:Recent investigations have elucidated some of the diverse roles played by reactive Oxygen and nitrogen species in events that lead to Oxygen Toxicity and defend against it. The focus of this review is on toxic and protective mechanisms in hyperoxia that have been investigated in our laboratories, with an emphasis on interactions of nitric oxide (NO) with other endogenous chemical species and with different physiological systems. It is now emerging from these studies that the anatomical localization of NO release, which depends, in part, on whether the Oxygen exposure is normobaric or hyperbaric, strongly influences whether Toxicity emerges and what form it takes, for example, acute lung injury, central nervous system excitation, or both. Spatial effects also contribute to differences in the susceptibility of different cells in organs at risk from hyperoxia, especially in the brain and lungs. As additional nodes are identified in this interactive network of toxic and protective responses, future advances may open up the possibility of novel pharmacological interventions to extend both the time and partial pressures of Oxygen exposures that can be safely tolerated. The implications of a better understanding of the mechanisms by which NO contributes to central nervous system Oxygen Toxicity may include new insights into the pathogenesis of seizures of diverse etiologies. Likewise, improved knowledge of NO-based mechanisms of pulmonary Oxygen Toxicity may enhance our understanding of other types of lung injury associated with oxidative or nitrosative stress.
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contributions of nitric oxide synthase isoforms to pulmonary Oxygen Toxicity local vs mediated effects
American Journal of Physiology-lung Cellular and Molecular Physiology, 2008Co-Authors: I T Demchenko, Claude A Piantadosi, Dmitriy N Atochin, Diana Gutsaeva, Ryan R Godfrey, Paul L Huang, Barry W AllenAbstract:Reactive species of Oxygen and nitrogen have been collectively implicated in pulmonary Oxygen Toxicity, but the contributions of specific molecules are unknown. Therefore, we assessed the roles of ...
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similar but not the same normobaric and hyperbaric pulmonary Oxygen Toxicity the role of nitric oxide
American Journal of Physiology-lung Cellular and Molecular Physiology, 2007Co-Authors: I T Demchenko, Barry W Allen, Karen E Weltywolf, Claude A PiantadosiAbstract:Pulmonary manifestations of Oxygen Toxicity were studied and quantified in rats breathing >98% O2 at 1, 1.5, 2, 2.5, and 3 ATA to test our hypothesis that different patterns of pulmonary injury wou...
Alan Leviton - One of the best experts on this subject based on the ideXlab platform.
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do clinical markers of barotrauma and Oxygen Toxicity explain interhospital variation in rates of chronic lung disease
Pediatrics, 2000Co-Authors: L Van Marter, Elizabeth N Allred, Marcello Pagano, Ulana Sanocka, Richard B Parad, Marianne Moore, Mervyn Susser, Nigel Paneth, Alan LevitonAbstract:OBJECTIVE To explore the hypothesis that variation in respiratory management among newborn intensive care units (NICUs) explains differences in chronic lung disease (CLD) rates. DESIGN Case-cohort study. SETTING NICUs at 1 medical center in New York (Babies' and Children's Hospital [Babies']) and 2 in Boston (Beth Israel Hospital and Brigham and Women's Hospital [Boston]). STUDY POPULATION Four hundred fifty-two infants born at 500 to 1500 g birth weight between January 1991 and December 1993, who were enrolled in an epidemiologic study of neonatal intracranial white matter disorders. CASE DEFINITION Supplemental Oxygen required at 36 weeks' postmenstrual age. RESULTS The prevalence rates of CLD differed substantially between the centers: 4% at Babies' and 22% at the 2 Boston hospitals, despite similar mortality rates. Initial respiratory management at Boston was more likely than at Babies' to include mechanical ventilation (75% vs 29%) and surfactant treatment (45% vs 10%). Case and control infants at Babies' were more likely than were those at Boston to have higher partial pressure of carbon dioxide and lower pH values on arterial blood gases. However, measures of Oxygenation and ventilator settings among case and control infants were similar at the 2 medical centers in time-oriented logistic regression analyses. In multivariate logistic regression analyses, the initiation of mechanical ventilation was associated with increased risk of CLD: after adjusting for other potential confounding factors, the odds ratios for mechanical ventilation were 13.4 on day of birth, 9.6 on days 1 to 3, and 6.3 on days 4 to 7. Among ventilated infants, CLD risk was elevated for maximum peak inspiratory pressure >25 and maximum fraction of inspired Oxygen = 1.0 on the day of birth, lowest peak inspiratory pressure >20 and maximum partial pressure of carbon dioxide >50 on days 1 to 3, and lowest white blood count <8 K on days 4 to 7. Even after adjusting for white blood count <8 K and the 4 respiratory care variables, infants in Boston continued to be at increased risk of CLD, compared with premature infants at Babies' Hospital. CONCLUSION In multivariate analyses, a number of specific measures of respiratory care practice during the first postnatal week were associated with the risk of a very low birth weight infant developing CLD. However, after adjusting for baseline risk, most of the increased risk of CLD among very low birth weight infants hospitalized at 2 Boston NICUs, compared with those at Babies' Hospital, was explained simply by the initiation of mechanical ventilation.
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do clinical markers of barotrauma and Oxygen Toxicity explain interhospital variation in rates of chronic lung disease
Pediatrics, 2000Co-Authors: L Van Marter, Elizabeth N Allred, Marcello Pagano, Ulana Sanocka, Richard B Parad, Marianne Moore, Mervyn Susser, Nigel Paneth, Alan LevitonAbstract:Objective. To explore the hypothesis that variation in respiratory management among newborn intensive care units (NICUs) explains differences in chronic lung disease (CLD) rates. Design. Case–cohort study. Setting. NICUs at 1 medical center in New York (Babies9 and Children9s Hospital [Babies9]) and 2 in Boston (Beth Israel Hospital and Brigham and Women9s Hospital [Boston]). Study Population. Four hundred fifty-two infants born at 500 to 1500 g birth weight between January 1991 and December 1993, who were enrolled in an epidemiologic study of neonatal intracranial white matter disorders. Case Definition. Supplemental Oxygen required at 36 weeks9 postmenstrual age. Results. The prevalence rates of CLD differed substantially between the centers: 4% at Babies9 and 22% at the 2 Boston hospitals, despite similar mortality rates. Initial respiratory management at Boston was more likely than at Babies9 to include mechanical ventilation (75% vs 29%) and surfactant treatment (45% vs 10%). Case and control infants at Babies9 were more likely than were those at Boston to have higher partial pressure of carbon dioxide and lower pH values on arterial blood gases. However, measures of Oxygenation and ventilator settings among case and control infants were similar at the 2 medical centers in time-oriented logistic regression analyses. In multivariate logistic regression analyses, the initiation of mechanical ventilation was associated with increased risk of CLD: after adjusting for other potential confounding factors, the odds ratios for mechanical ventilation were 13.4 on day of birth, 9.6 on days 1 to 3, and 6.3 on days 4 to 7. Among ventilated infants, CLD risk was elevated for maximum peak inspiratory pressure >25 and maximum fraction of inspired Oxygen = 1.0 on the day of birth, lowest peak inspiratory pressure >20 and maximum partial pressure of carbon dioxide >50 on days 1 to 3, and lowest white blood count Conclusion. In multivariate analyses, a number of specific measures of respiratory care practice during the first postnatal week were associated with the risk of a very low birth weight infant developing CLD. However, after adjusting for baseline risk, most of the increased risk of CLD among very low birth weight infants hospitalized at 2 Boston NICUs, compared with those at Babies9 Hospital, was explained simply by the initiation of mechanical ventilation.
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clinical markers of barotrauma and Oxygen Toxicity and inter hospital variation in rates of chronic lung disease among surviving very low birth weight infants
Pediatric Research, 1999Co-Authors: L Van Marter, Alan Leviton, Elizabeth N Allred, Marcello Pagano, Ulana Sanocka, Richard B Parad, Marianne MooreAbstract:Clinical Markers of Barotrauma and Oxygen Toxicity and Inter-Hospital Variation in Rates of Chronic Lung Disease Among Surviving Very Low Birth Weight Infants
Jay B Dean - One of the best experts on this subject based on the ideXlab platform.
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toward a soft computing based correlation between Oxygen Toxicity seizures and hyperoxic hyperpnea
Soft Computing, 2018Co-Authors: Gianni Dangelo, Raffaele Pilla, Jay B Dean, Salvatore RamponeAbstract:Exposure to high levels of hyperbaric Oxygen ( $$\hbox {HBO}_{2}$$ ) can induce central nervous system Oxygen Toxicity in humans and animals, a phenomenon characterized by repeated tonic–clonic seizures. The risk of developing this type of convulsions represents the limiting factor in using $$\hbox {HBO}_{2}$$ for a number of clinical and diving applications. Previously, using radio-telemetry in awake rats, a significant increase in the mean value of the ventilatory responses in rats to $$\hbox {HBO}_{2}$$ approximately 5–8 min before onset of seizures has been observed. This response has been termed “hyperoxic hyperpnea,” and it has been hypothesized it may serve as a predictor of an impending seizure while breathing $$\hbox {HBO}_{2}$$ . The purpose of the present study was to apply soft computing methods to determine whether there is a direct correlation between the onset of hyperoxic hyperpnea (i.e., the ventilatory response as defined by tidal volume and respiratory frequency) and the onset of seizure. In our experiments, we used Multilayer Perceptron, Naive Bayes, J48, and U-BRAIN aimed at evidencing the correlation between the respiratory feature vectors and the onset of an impending seizure in unanesthetized, freely behaving rats breathing 4, 5 or 6 atmospheres absolute (ATA) of Oxygen. This strategy was also aimed to finding a set of rules relating physiological parameters and convulsive phenomena through inductive inference.
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therapeutic ketosis with ketone ester delays central nervous system Oxygen Toxicity seizures in rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2013Co-Authors: Dominic P Dagostino, Raffaele Pilla, Heather E Held, Carol S Landon, Michelle Puchowicz, Henri Brunengraber, Csilla Ari, Patrick Arnold, Jay B DeanAbstract:Central nervous system Oxygen Toxicity (CNS-OT) seizures occur with little or no warning, and no effective mitigation strategy has been identified. Ketogenic diets (KD) elevate blood ketones and have successfully treated drug-resistant epilepsy. We hypothesized that a ketone ester given orally as R,S-1,3-butanediol acetoacetate diester (BD-AcAc(2)) would delay CNS-OT seizures in rats breathing hyperbaric Oxygen (HBO(2)). Adult male rats (n = 60) were implanted with radiotelemetry units to measure electroencephalogram (EEG). One week postsurgery, rats were administered a single oral dose of BD-AcAc(2), 1,3-butanediol (BD), or water 30 min before being placed into a hyperbaric chamber and pressurized to 5 atmospheres absolute (ATA) O2. Latency to seizure (LS) was measured from the time maximum pressure was reached until the onset of increased EEG activity and tonic-clonic contractions. Blood was drawn at room pressure from an arterial catheter in an additional 18 animals that were administered the same compounds, and levels of glucose, pH, Po(2), Pco(2), β-hydroxybutyrate (BHB), acetoacetate (AcAc), and acetone were analyzed. BD-AcAc(2) caused a rapid (30 min) and sustained (>4 h) elevation of BHB (>3 mM) and AcAc (>3 mM), which exceeded values reported with a KD or starvation. BD-AcAc(2) increased LS by 574 ± 116% compared with control (water) and was due to the effect of AcAc and acetone but not BHB. BD produced ketosis in rats by elevating BHB (>5 mM), but AcAc and acetone remained low or undetectable. BD did not increase LS. In conclusion, acute oral administration of BD-AcAc(2) produced sustained ketosis and significantly delayed CNS-OT seizures by elevating AcAc and acetone.
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a potential early physiological marker for cns Oxygen Toxicity hyperoxic hyperpnea precedes seizure in unanesthetized rats breathing hyperbaric Oxygen
Journal of Applied Physiology, 2013Co-Authors: Raffaele Pilla, Carol S Landon, Jay B DeanAbstract:Hyperbaric Oxygen (HBO2) stimulates presumptive central CO2-chemoreceptor neurons, increases minute ventilation (Vmin), decreases heart rate (HR) and, if breathed sufficiently long, produces centr...
Barry W Allen - One of the best experts on this subject based on the ideXlab platform.
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two faces of nitric oxide implications for cellular mechanisms of Oxygen Toxicity
Journal of Applied Physiology, 2009Co-Authors: Barry W Allen, I T Demchenko, Claude A PiantadosiAbstract:Recent investigations have elucidated some of the diverse roles played by reactive Oxygen and nitrogen species in events that lead to Oxygen Toxicity and defend against it. The focus of this review is on toxic and protective mechanisms in hyperoxia that have been investigated in our laboratories, with an emphasis on interactions of nitric oxide (NO) with other endogenous chemical species and with different physiological systems. It is now emerging from these studies that the anatomical localization of NO release, which depends, in part, on whether the Oxygen exposure is normobaric or hyperbaric, strongly influences whether Toxicity emerges and what form it takes, for example, acute lung injury, central nervous system excitation, or both. Spatial effects also contribute to differences in the susceptibility of different cells in organs at risk from hyperoxia, especially in the brain and lungs. As additional nodes are identified in this interactive network of toxic and protective responses, future advances may open up the possibility of novel pharmacological interventions to extend both the time and partial pressures of Oxygen exposures that can be safely tolerated. The implications of a better understanding of the mechanisms by which NO contributes to central nervous system Oxygen Toxicity may include new insights into the pathogenesis of seizures of diverse etiologies. Likewise, improved knowledge of NO-based mechanisms of pulmonary Oxygen Toxicity may enhance our understanding of other types of lung injury associated with oxidative or nitrosative stress.
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contributions of nitric oxide synthase isoforms to pulmonary Oxygen Toxicity local vs mediated effects
American Journal of Physiology-lung Cellular and Molecular Physiology, 2008Co-Authors: I T Demchenko, Claude A Piantadosi, Dmitriy N Atochin, Diana Gutsaeva, Ryan R Godfrey, Paul L Huang, Barry W AllenAbstract:Reactive species of Oxygen and nitrogen have been collectively implicated in pulmonary Oxygen Toxicity, but the contributions of specific molecules are unknown. Therefore, we assessed the roles of ...
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similar but not the same normobaric and hyperbaric pulmonary Oxygen Toxicity the role of nitric oxide
American Journal of Physiology-lung Cellular and Molecular Physiology, 2007Co-Authors: I T Demchenko, Barry W Allen, Karen E Weltywolf, Claude A PiantadosiAbstract:Pulmonary manifestations of Oxygen Toxicity were studied and quantified in rats breathing >98% O2 at 1, 1.5, 2, 2.5, and 3 ATA to test our hypothesis that different patterns of pulmonary injury wou...
