Reduced nitric oxide concentration in exhaled gas after exposure to hyperbaric hyperoxia (original) (raw)
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Pulmonary Oxygen Toxicity Through Exhaled Breath Markers After Hyperbaric Oxygen Treatment Table 6
Frontiers in Physiology
Introduction: The hyperbaric oxygen treatment table 6 (TT6) is widely used to manage dysbaric illnesses in divers and iatrogenic gas emboli in patients after surgery and other interventional procedures. These treatment tables can have adverse effects, such as pulmonary oxygen toxicity (POT). It is caused by reactive oxygen species’ damaging effect in lung tissue and is often experienced after multiple days of therapy. The subclinical pulmonary effects have not been determined. The primary aim of this study was to measure volatile organic compounds (VOCs) in breath, indicative of subclinical POT after a TT6. Since the exposure would be limited, the secondary aim of this study was to determine whether these VOCs decreased to baseline levels within a few hours.Methods: Fourteen healthy, non-smoking volunteers from the Royal Netherlands Navy underwent a TT6 at the Amsterdam University Medical Center—location AMC. Breath samples for GC-MS analysis were collected before the TT6 and 30 min...
American Journal of Physiology-Lung Cellular and Molecular Physiology, 2007
Pulmonary manifestations of oxygen toxicity were studied and quantified in rats breathing >98% O2at 1, 1.5, 2, 2.5, and 3 ATA to test our hypothesis that different patterns of pulmonary injury would emerge, reflecting a role for central nervous system (CNS) excitation by hyperbaric oxygen. At 1.5 atmosphere absolute (ATA) and below, the well-recognized pattern of diffuse pulmonary damage developed slowly with an extensive inflammatory response and destruction of the alveolar-capillary barrier leading to edema, impaired gas exchange, respiratory failure, and death; the severity of these effects increased with time over the 56-h period of observation. At higher inspired O2pressures, 2–3 ATA, pulmonary injury was greatly accelerated but less inflammatory in character, and events in the brain were a prelude to a distinct lung pathology. The CNS-mediated component of this lung injury could be attenuated by selective inhibition of neuronal nitric oxide synthase (nNOS) or by unilateral ...
Effects of a standard hyperbaric oxygen treatment protocol on pulmonary function
European Respiratory Journal, 1998
Recompression and hyperbaric oxygen (HBO) are used in the treatment for diving-related diseases such as decompression sickness and arterial gas embolism. For a long time HBO has also been shown to be effective in carbon monoxide poisoning and anaerobic infections. More recently, HBO has been shown to have supplementary effects in the treatment of other disorders characterized by local ischaemia. An increase in local oxygen supply due to an increased gradient for diffusion is achieved by increasing the partial pressure of oxygen (PO 2 ) in inspired gas. This results in local stimulation of fibroblast proliferation and collagen synthesis, angiogenesis and enhanced granulocyte function and peroxidase activity in ischaemic tissue. In this way, HBO treatment is an effective adjunct in the treatment of osteoradionecrosis, chronic osteomyelitis, diabetic leg ulcers and radiation-induced proctitis and cystitis. On an experimental basis, HBO treatment is currently evaluated as a supplement in the treatment of several other disorders. Indications for HBO treatment have been worked out by the Undersea and Hyperbaric Society [1], differentiating between indications where HBO has been shown to have a definite effect based on controlled clinical studies and indications where HBO still has to be considered experimental. In this setting, HBO treatment is usually given for 90 min daily at a PO 2 of 200-280 kPa for 20-30 days.
Effects of hyperbaric oxygen on nitric oxide generation in humans
Nitric Oxide, 2015
Background: Hyperbaric oxygen (HBO2) has been suggested to affect nitric oxide (NO) generation in humans. Specific NO synthases (NOSs) use L-arginine and molecular oxygen to produce NO but this signaling radical may also be formed by serial reduction of the inorganic anions nitrate and nitrite. Interestingly, commensal facultative anaerobic bacteria in the oral cavity are necessary for the first step to reduce nitrate to nitrite. The nitrate-nitrite-NO pathway is greatly potentiated by hypoxia and low pH in contrast to classical NOS-dependent NO generation. We investigated the effects of HBO2 on NO generation in healthy subjects including orally and nasally exhaled NO, plasma and salivary nitrate and nitrite as well as plasma cGMP and plasma citrulline/ arginine ratio. In addition, we also conducted in-vitro experiments in order to investigate the effects of hyperoxia on nitrate/nitrite metabolism and NO generation by oral bacteria. Methods: Two separate HBO2 experiments were performed. In a cross-over experiment (EXP1) subjects breathed air at 130 kPa (control) or oxygen at 250 kPa for 100 minutes and parameters were measured before and after exposure. In experiment 2 (EXP 2) measurements were performed also during HBO2 at 250 kPa for 110 minutes. Results: HBO2 acutely reduced orally and nasally exhaled NO by 30% and 16%, respectively. There was a marked decrease in salivary nitrite/nitrate ratio during and after HBO2, indicating a reduced bacterial conversion of nitrate to nitrite and NO. This was supported by in vitro experiments with oral bacteria showing that hyperoxia inhibited bacterial nitrate and nitrite reduction leading to reduced NO generation. Plasma nitrate was unaffected by HBO2 while plasma nitrite was reduced during HBO2 treatment. In contrast, plasma cGMP increased during HBO2 as did citrulline/arginine ratio after treatment and control. Conclusion: HBO2-exposure in humans affects NO generation in the airways and systemically differently. These data suggest that the individual NOSs as well as the nitrate-nitrite-NO pathway do not respond in a similar way to HBO2.
American Journal of Respiratory and Critical Care Medicine, 1997
Nitric oxide (NO) may either protect against or contribute to oxidant-induced lung injury. In this study, we sought to determine whether either inhaled NO in concentration of 10 and 100 parts per million (ppm) or inhibition of endogenous NO formation with L-NG nitroarginine methyl ester (L-NAME) or aminoguanidine alters the extent of lung injury in rats breathing 100% 0 2. Lung thiobarbituric acid reactive substances (TBARS), wet to dry lung weight ratio (Q W/QD), vascular and epithelial permeability (assessed by simultaneous intravenous administration of 131 1-labeled albumin and intraalveolar instillation of 125 1-labeled albumin), alveolar liquid clearance (evaluated based on the increase in alveolar protein concentration), and lung liquid clearance (gravimetric method) were determined after 40 h exposure to either 100% or 21% 0 2 . Exposure to hyperoxia caused increases in lung TBARS from 10.5 ± 0.7 to 13.7 ± 1.5 µmol/mg protein (p < 0.05); in blood hemoglobin concentration (Hb) from 14 ± 1 g/dI to 17 ± 1 g/d1 (p < 0.05); in the QW/QD ratio from 4.02 ± 0.3 to 5.31 ± 0.5 (p < 0.05); and in alveolar-arterial oxygen tension difference from 124 ± 14 mm Hg to 241 ± 61 mm Hg (p < 0.05); as well as a decrease in blood pressure, from 131 ± 15 mm Hg to 72 ± 26 mm Hg (p < 0.05). Hyperoxia also increased vascular albumin leakage and moderately altered epithelial barrier permeability to protein. Inhalation of 10 ppm NO prevented the increases in TBARS and QW/QD, had no effect on the alveolar barrier impermeability to protein, and improved alveolar liquid clearance. Inhalation of 100 ppm NO did not alter the increases in TBARS and QW/QD but increased vascular permeability to protein. Survival of rats exposed to hyperoxia was not improved by inhaled NO. Treatment with L-NAME or aminoguanidine reduced survival. L-NAME, but not aminoguanidine, increased lung TBARs. These results suggest that, depending on its concentration, inhaled NO can either reduce or increase the early consequences of hyperoxic lung injury. Treatment with L-NAME, and to a lesser extent aminoguanidine, worsened hyperoxic lung injury, indicating a protective effect of endogenous NO. Garat C, Jayr C, Eddahibi S, Laffon M, Meignan M, Adnot S. Effects of Inhaled nitric oxide or Inhibition of endogenous nitric oxide formation on hyperoxic lung Injury.
High-dose Nitric Oxide Inhalation Increases Lung Injury after Gastric Aspiration
Anesthesiology, 1999
Background-Inhaled nitric oxide is often used in patients with adult respiratory distress syndrome. However, nitric oxide also may be significantly toxic, especially if administered concurrently with hyperoxia. The authors evaluated the isolated effect of nitric oxide and the combined effects of nitric oxide and hyperoxia on lung injury in rats after acid aspiration.
Mechanisms of protection against pulmonary hyperbaric O2 toxicity by intermittent air breaks
European Journal of Applied Physiology, 2008
Intermittent exposure to air is used as a protective strategy against hyperbaric O 2 (HBO 2) toxicity. Little is known about optimal intermittent exposure schedules and the mechanism of protection. In this study, we examined the role of antioxidant enzymes, and inXammatory cytokines in the mechanism of HBO 2 tolerance by intermittent air breaks. One group of rats was exposed continuously to 282 kPa O 2 until death. Other groups were exposed to 30, 60, and 120 min intervals of HBO 2 with diVerent numbers of intermittent 30 min air breaks (1-12 breaks). After the Wnal break, animals were exposed to HBO 2 until death. In a separate experiment, animals were sacriWced before terminal exposure and lung tissues were collected for analysis of gene expression. Two intermittent schedules with 6 h cumulative O 2 time (30/30 and 60/30 min schedules) were compared with continuous exposure to HBO 2 for 6 h and with intermittent exposure of 8 h (120/30 min schedule) duration. Continuous exposure resulted in activation of inXammatory cytokine TNF-and IL-1 mRNA expression, an increase in lung protein nitration and activation of inducible NOS (iNOS) mRNA. InXammatory response was not observed at intermittent exposures of the same cumulative O 2 time duration (30/30 and 60/30 min schedule). Expression of heme oxygenase-1 (HO-1) mRNA was sig-niWcantly increased in all exposure groups while manganese superoxide dismutase (MnSOD) mRNA expression was increased only in continuous and 120/30 exposure groups. Results show that intermittent exposure to air protects against pulmonary HBO 2 toxicity by inhibiting inXammation. The mechanism of inhibition may involve the antiinXammatory and antioxidative eVect of HO-1 but some other mechanisms may also be involved in protection by intermittent air breaks.
Folia Medica, 2016
Introduction: Exogenous hypoxia increases ventilation and contracts the pulmonary vessels. Whether those factors change the values of nitric oxide in exhaled air has not yet been evaluated. Objective: To examine the effect of exogenous normobaric hypoxia on the values of the fraction of nitric oxide in exhaled breath (FeNO). Subjects аnd Methods: Twenty healthy non-smoker males at mean age of 25.4 (SD = 3.7) were tested. The basal FeNO values were compared with those at 7 min. and 15 min. after introducing into the hypoxic environment (hypoxic tent), imitating atmospheric air with oxygen concentration corresponding to 3200 m above sea level. Exhaled breath temperature was measured at baseline and at 10-12 min. of the hypoxic exposition. Heart rate and oxygen saturation were registered by pulse-oximetry. Results: All the subjects had FeNO values in the reference range. The mean baseline value was 14.0 ± 3.2 ppb, and in hypoxic conditions - 15.5 ± 3.8 ppb (7 min.) and 15.3 ± 3.6 ppb (...
Effects on pulmonary function of daily exposure to dry or humidified hyperbaric oxygen
Respiration Physiology, 1997
The purpose of this study was to examine the effects of breathing dry or humidified hyperbaric oxygen on pulmonary function. Pulmonary function tests were performed before and after each of 10 hyperbaric oxygen exposures at 2.5 atmospheres absolute (ATA) for 95 min in a group of 13 patients treated daily by hyperbaric oxygen for problem wounds. Patients breathed dry oxygen during five successive sessions and humidified oxygen during the remaining five. No differences were found between forced vital capacities (FVC) and maximal expiratory flows before and after hyperbaric oxygen exposure while breathing dry or humidified oxygen. Significant differences were found for the changes in the percentage of FVC expired in 1 s (FEV 1% ) and mean forced mid-expiratory flow rate during the middle half of the FVC (FEF 25 -75% ) on day 1 alone: decrements of 1.42 and 2.96%, respectively, under dry oxygen, vs. increments of 3.93 and 34.4%, respectively, for humidified oxygen. Day-to-day decrements in the percent changes in FEV 1% and FEF 25 -75% were observed while breathing humidified hyperbaric oxygen. These results demonstrate that repeated daily exposure to humidified hyperbaric oxygen abolishes the initial beneficial effect of humidification on peripheral airways flow characteristics. © 1997 Elsevier Science B.V.
2013
Copyright © 2011 William J. Mach et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Oxygen (O2) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hyperoxia-induced reactive O2 species (ROS) which may readily react with surrounding biological tissues, damaging lipids, proteins, and nucleic acids. Protective antioxidant defenses can become overwhelmed with ROS leading to oxidative stress. Activated alveolar capillary endothelium is characterized by increased adhesiveness causing accumulation of cell populations such as neutrophils, which are a source of ROS. Increased levels of ROS cause...