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Resumen A pesar de las referencias que advierten sobre los efectos adversos de la utilización de O2 suplementario sin asistencia ventilatoria en pacientes con enfermedades neuromusculares (ENM), aún hoy continúan ingresando pacientes en unidades de cuidados intensivos con hipercapnia grave y narcosis por CO2. Parecería que el problema es redescubierto según pasan los años y las generaciones. Muchos pacientes y su red de cuidadores formales e informales no son conscientes de este riesgo que puede llevar a un empeoramiento significativo de los síntomas, eventos agudos, ingresos hospitalarios y, en algunos casos, causar la muerte. Este artículo está centrado en los riesgos de la administración de O2, así como en sus indicaciones puntuales en personas con ENM. El problema central es que la administración de O2 puede quitar el impulso hipóxico para ventilar, aunque otros mecanismos podrían estar involucrados. El retiro completo de la oxigenoterapia sin apoyo de asistencia ventilatoria, es un error aún mayor. Es posible administrar O2 y controlar el CO2 de forma segura. Nunca se debe administrar O2 sin monitorear constantemente el nivel de CO2. La ventilación no invasiva binivelada (BiPAP) mediante interfaz nasal, bucal o boquilla, es la principal medida para revertir la hipoventilación y lograr el descenso de la PaCO2. Las indicaciones de oxigenoterapia en personas con ENM han sido consensuadas y están reservadas a situaciones específicas. Para mejorar la atención de aquellos enfermos con ENM y evitar intervenciones iatrogénicas, se requiere educación al equipo de salud y contención en el entorno del paciente.
Abstract Although the references warn about the adverse effects of adding O2 without ventilatory assistance in patients with neuromuscular diseases (NMD), patients are still to be admitted to intensive care units with severe hypercapnia and CO2 narcosis. It seems that the problem is rediscovered as the years and generations go by. Unfortunately, many patients and their network of formal and informal caregivers are unaware of this risk, leading to significant worsening of symptoms, acute events, hospital admissions, and, in some cases, cause death. This article focuses on the dangers of O2 administration as well as its precise indications in people with NMD. The central problem is that the administration of O2 can remove the hypoxic impulse to ventilate, however, other mechanisms could be involved, but. The complete withdrawal of oxygen therapy is an even greater mistake if it is not supported by ventilatory assistance. It is possible to supply O2 and control CO2 safely. Oxygen should never be administered without constantly monitoring the CO2 level. Bi-level non-invasive ventilation (BiPAP) through a buccal, nasal interface or mouthpiece is the primary measure to reverse hypoventilation and achieve a decrease in PaCO2. The indications for oxygen therapy in people with NMD have been agreed upon and are reserved for specific situations. To improve the care of those with NMD and avoid iatrogenic interventions, education of the health team and support in the patient's environment is required.
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@#A diving decompression procedure is a specific rule that divers should follow when they ascend and get out of water. It comes from the decompression theory and algorithm and is designed for the prevention of decompression sickness. With the ， ， development of diving technology and diving medicine the decompression procedures are constantly innovated and the new ， decompression procedure can be used in diving practice after safety verification. In principle the safety verification of ， decompression procedures should be conducted on animal experiments before human experiments and the risks of ， decompression sickness and oxygen toxicity should be systematically assessed. However the assessment methods used in ， ， ， different studies differ greatly thus it is urgent to establish a standard and universal verification system. Traditionally the risk ， ， assessment of decompression sickness and oxygen toxicity is mainly carried out by observing the incidence detecting bubbles ， theoretical calculation and lung functional test. Furthermore biochemical indicators are increasingly becoming important ， ， supplements. Due to the special underwater environment the diving operation is prone to accidents. Therefore in addition to ， verifying the safety of the new decompression procedure exploring its safety decompression limit is of great significance for the formulation of emergency decompression procedures in emergency situations. The specific approach is to shorten the decompression time and assess the safety until the critical time for detecting bubbles without the occurrence of decompression ， ， sickness is found. Future studies should continue to optimize safety assessment methods explore sensitive biochemical markers ， clarify species associations and improve verification efficiency and reliability of results.
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Hyperbaric oxygen has been widely used in the treatment of many diseases and in some special circumstances such as deepwater diving, and it plays an irreplaceable role. But oxygen toxicity is an important complication, especially in diving medicine. Due to the characteristics of lung itself and the differences in dry/wet environment, the pathological mechanism of pulmonary oxygen toxicity is very complicated. With the advances in the experimental techniques and expansion of the research ideas, the studies on pulmonary oxygen toxicity have no longer limited to the level of tissue morphology and pathological strata, more and more studies that focused on cellular and sub-cellular levels have been carried out. The present review will focus mainly on the clinical manifestations, pathophysiology, pathogenesis and progresses in monitoring and treatment of pulmonary oxygen toxicity over recent years.
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Background Retinal flatmount of oxygen-induced retinopathy (OIR) animal models is a useful tool in the study of ischemic retinopathy.The retinas of OIR of rat or mouse pups were small and thick and difficult in operating of conventional preparation and quantitative analysis of retinal flatmounts.Objective This study was to explore an easy and stable operating method of retinal flatmount combined with immunofluorescence staining in rodent.Methods Forty ＜6-hour-old SD rat pups were randomly assigned to OIR model group and normal control group.The pups were raised with nursing mothers in hyperoxia environment (80％) and normal oxygen environment (21％) alternately at a 24-hour interval for 14 days in the OIR model group,and the pups were raised in the room air for 14 days in the normal control group.The eyeballs of the rats were extracted to isolate the retinas intactly.The retinas were stained with glutamine synthetase (GS)-isolectin B4 firstly and then expanded into flatmounted and cut into 4 petals radially.Adobe Photoshop CS3 imaging analysis system was used to match the pictures into entire retinal vascular images and analyzed under the fluorescence microscope.The pixel values of retinal avascular areas and the entire retina were quantified by this system.The percentage of avascular areas to the entire retina was calculated to analyze the severity of non-perfusion areas.The use and care of the animals complied with the Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission.Results An intact and smooth retinal flatmount could be obtained by firstly staining method.Ora serrata structure was seen surrounding the whole retina.Strong green fluorescence was exhibited in retinal vessel net with clearly visible vascular branches;while the background fluorescence was weaker.Fully developed blood vessels were displayed in the retinas of the normal control group.Non-capillary areas around the central optic disk and large peripheral avascular areas could be seen in the retinal flatmounts of OIR models.Conclusions The preparation of retinal flatmount is easy and feasible by first immunofluorescence staining for retinal vessels followed by radially cutting of retina.This method of retinal flatmount can ensure the integrity of retinal vascular system and it is available for the observation and evaluation of retinal vascular structure in OIR models.
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Background Retinal neovascularization is associated with various disorders.Studying the pathogenesis of retinal neovascularization is of important significance.Oxygen-induced retinopathy(OIR) mouse model is a common animal model for the study of retinal neovascular diseases.However, conventional modeling methods usually cause high animal mortality and low rate of success.Objective This study aimed to establish a modified method of mouse OIR model.Methods Eighty 1-week-old SPF C57BL/6J mice were randomly divided into normal control group and OIR group with 40 mice for each.The newborn mice of the normal control group were kept in a normal air environment with their breast-feeding mothers, but the mice of postnatal 2 days (P2) in the OIR group were raised with two litters per cage until P7.The P7 mice exposed to oxygen tank containing 80％ oxygen together with one or another mother mouse alternately daily for 5 days and then returned to the normal air environment.The success rate of modeling,mortality rate of maternal mice and survival rate of immature mice were evaluated.The mixed solution of fluorescein isothiocyanate (FITC) and PBS with 4％ paraformaldehyde was infused into the hearts of P12, P14,P17 and P21 mice and the eyeballs were obtained after the mice were sacrificed for histopathological examination of retinas and preparation of retinal flatmounts.The number of vascular endothelial cells extending inner limiting membrane was counted and the distribution of retinal vessels was evaluated.The use and care of the animals complied with the Statement of ARVO.Results The survival rate of the neonatal mice was 100％ both in the normal control group and the OIR group,and the survival rate of maternal mice was 85.7％ in the OIR group.Retinal new vessels were found in the mice of the OIR group,with the success rate of modeling 100％.The retinal vessels distributed from optical disc toward periphery in P14 mice in the normal group.However,in the OIR group,non-perfusion area at the posterior pole was seen in P12 mice,new blood vessels at the periphery were found in P14 mice, neovascularization at the junction area between vascular area and non-perfusion area as well as leakages were exhibited in P17 mice,and less non-perfusion area and new vessels were seen in P21 mice.Retinal inner limiting membrane was smooth in the mice of the normal group, and the vascular endothelial cell nucleus extending inner limiting membrane were seen in P12 mice and peaked in P17 mice.The vascular endothelial cell nucleus were (11.44±2.01), (31.24±1.50) and (9.23-±1.12)/slide in P14, P17 and P21 mice in the OIR group,which were significantly more than (0.27±0.14) , (0.30±0.11) and (0.32±0.16)/slide in P14, P17 and P21 mice in the normal group (t=47.90,61.30,40.70,all at P＜0.05).Conclusions The method of OIR modeling is modified by alternating maternal mice,exposing to 80％ oxygen-nitrogen mixture gas and cohabitating immature mice.Modified modeling method is simple with the low death rate of maternal mice and stable OIR phenotype.
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Objective To investigate the effect of PPAR-δ on the lung injury of rats induced by hyperbaric oxygen (HBO2) exposure.Methods Sixty male Sprague-Dawley rats were randomly divided into six groups:air+vehicle, air+GW0742, and air+GSK0660, HBO2 +vehicle, HBO2 +GW0742, HBO2 +GSK0660.Lung injury was induced in rats by HBO2exposure (2.3 ATA, 100%O2, 8 h).Rats were injected with vehicle[10%DMSO in 0.3 ml NaCl 0.9%(v/v)] or GW0742 (0.3 mg/kg, ip) or GSK0660 (1 mg/kg, ip) at 1, 6 and 12 hours before either air or oxygen exposure .Protein levels in the bronchoalveolar lavage fluid ( BALF) , wet/dry ratio of the lung and the pathological changes in the lung tissue were detected 30 min after rats′egress.Results and Conclusion For the HBO2 +GW0742 group, the protein levels in BALF, the wet/dry ratio of the lung and the pathological changes in lung tissues all significantly decreased compared with those of the air group .These changes in HBO 2 +GSK0660 group tended to increase the level of lung injury .PPAR-δhas a protective effect on pulmonary oxygen toxicity induced by HBO 2 .
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The class of Actinobacteria is a large group of gram-positive bacteria and having high G+C content. Actinobacteria also produced curious compound like thiols mainly Mycothiol (MSH) and Glutathione (GSH). MSH is also known as mycothiol and comprised of a cysteine residue with an acetylated amino group which is linked to glucosamine to inositol but Glutathione (GSH) having gamma peptide linkage between cysteine group which is attached by normal peptide linkage to a glycine and the carboxyl group of the glutamate side-chain. These thiols play a key role in maintaining a reducing environment in the cell, which is necessary for regular metabolic activities and represent adaptation under stress condition for survival of organisms. Both Mycothiol and glutathione (GSH) having property to protect cells against oxygen toxicity but MSH shows 7 fold slower ability to resistance of autoxidation compare to GSH but GSH is absent in archaebacterium and rarely found in Streptomycetes strains (Streptomyces lactamdurans). In this review article we discussed about the GSH and MSH structure, properties and how GSH is better than MSH in the case of antioxidant production.
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PURPOSE: Pulmonary oxygen toxicity is mainly an inflammatory process, triggered by reactive oxygen species via a number of biochemical pathways. Recent evidence implies that ROS may stimulate NF-Kb to promote the synthesis of genes for inflammatory cytokines. At the same time, corticosteroids have been implicated in the prevention of activating this step. However, adverse reactions of systernic corticosteroids cause physicians to hesitate their use, not to mention their doubtful effectiveness. Budesonide is a locally acting corticosteroid with little systemic effect. Inhaled either through nebulizers or metered dose inhalers, it has proved the antiinflammatory, and thus antiasthmatic, effects in patients with asthma. If oxygen-induced injury is mediated by factors involved in a similar pathway as described above, budesonide will have protective effects against inflammatory responses of pulmonary oxygen toxicity. METHODS: We used 10 adult mice in each of the three groups, AC is the room air control group, OC is the oxygen control group in which mice were exposed to 95% oxygen for 48 h; and TX is the treatment group in which mice were exposed to 95% oxygen for 48 h, and during that period they were given budesonide via a nebulizer 500 p g/dose every 12 h for 4 times. The mice were sacrificed with iection of a lethal dose of ketamine. Tracheotomy was done and an 18G ET tube was inserted. The lungs were lavaged with 80 ml/kg(or 80 microliter/g) isotonic saline slowly injected through the ET tube. The lung lavage fluid was centrifuged at 8000 rpm for 2 rninutes. Supernatant was used for analysis of IL-6, while the precipitate was resuspended in 200 microliter of isotonic saline for cell count. RESULTS: The simple mean IL-6 values did not show a significant difference between groups (AC 199.4+/-192.7; OC 274.5+/-31.3; and TX 269.8+/-127.G pg/Ml). But considering their skewed distribution in AC and TX groups, the median values showed a conspicuous difference among 3 groups, that is, the median IL-6 value of AC was 124.8 pg/Ml, OC 269.8 pg/Ml, and TX 217.4 pglmL. For the cell counts, AC was 189+/-56/mm, OC 424+/-111/mm, and TX 266+/-22/mm(P<0.05). CONCLUSION: In conclusion, budesonide nebulization appears to have protective effects against inflammatory responses of pulmonary oxygen toxicity in adult mice.
Subject(s)
Adult , Animals , Humans , Mice , Adrenal Cortex Hormones , Asthma , Bronchoalveolar Lavage Fluid , Bronchoalveolar Lavage , Budesonide , Cell Count , Cytokines , Interleukin-6 , Ketamine , Lung , Metered Dose Inhalers , Nebulizers and Vaporizers , NF-kappa B , Oxygen , Reactive Oxygen Species , TracheotomyABSTRACT
Prolonged exposure to hyperoxia has been associated with progressive injury to the alveolar-capillary membrane, leading to increased alveolar and pulmonary vascular permeability, pulmonary edema, atelectasis, and eventual death from hypoxemia, hypercapnia and/or metabolic acidemia. Several constitutional and environmental factors may also influence tolerance to hyperoxia. Among factors best explored experimentally are metabolic, diet, medications and chemicals, and prior exposure to hyperoxia or hypoxia. Many animal models of increased oxygen tolerance have been investigated, but to date no clinically useful means of reducing oxygen-induced lung injury in human exists. To this point, this study was designed to study the effect of previous exposure to 100% oxygen on the pulmonary oxygen toxicity during the following exposure to 100% oxygen. Eighty female Wistar rats were partitioned into five groups(n=16 for each group): Gr. I is control exposed to room air; Gr. II breathed 100% O2 for 2 days and room air for 1 day; Gr. III, IV and V breathed 100% O2 for 2 days, room air for 1 day, and then each group was exposed to 100% O for I, 3 and 5 days, respectively. All groups were partitioned into 2 sub-groups (n=8 for each subgroup): One sub-group for studing (125)I-albumin flux ratio, superoxide dismutase(SOD) activity in blood, and lung and body weight; the other sub-group for studing lung-thorax compliance, and analyzing bonchoalveolar lavage(BAL) fluid. Only two rats in Gr. V were dead. Body weight was significantly lower(p<0.05) in Gr. V compared to the other groups. Percent lung weight of total body weight for wet and dry lungs in Gr. IV and V were higher (p<0.05) than those in Gr. I, II and III. In contrast, mean wet lung/dry lung ratio were not changed in each group. Inflation lung-thorax compliances were lower(p<0.05) in Gr. II, III, IV and V, but deflation lung-thorax compliances were not changed. (125)I-albumin flux ratio was greater(p<0.05) in Gr. IV and V than those in Gr. I, II and III. Albumin concentrations in BAL was increased in Gr II, III, IV and V and albumin ratio of BAL/plasma was increased in Gr II, III, IV and V. Lactic dehydrogenase(LDH) was greater (p<0.05) in Gr. IV and V. Alkaline phosphatase was increased (p<0.05) only in group IV. Dry lung and wet lung weights were increased and body weight were decreased proportionally to the increase in (125)I-albumin flux ratio. This study suggested that pre-treatment with 100% oxygen for 2 days and exposure to room air for 1 day increase survival rate and tolerance to pulmonary oxygen toxicity in the following exposure to high concentration of oxygen. The mechanisms of increased tolerance should be searched in the further biochemical studies, including anti-oxidant enzyme systems.
Subject(s)
Animals , Female , Humans , Rats , Alkaline Phosphatase , Hypoxia , Body Weight , Capillary Permeability , Compliance , Diet , Hypercapnia , Hyperoxia , Inflation, Economic , Lung , Lung Injury , Membranes , Models, Animal , Oxygen , Pulmonary Atelectasis , Pulmonary Edema , Rats, Wistar , Superoxides , Survival Rate , Weights and MeasuresABSTRACT
Animal study was performed to determine the changes in rat lung permeability in hyperoxic condition. 3 groups of rats (n=8 each) were exposed to 100% oxygen for 24 hr(group 2), 48 hr(group 3) and 72 hr(group 4), respectively, and compared with control (group 1 at room air, n=8). The time course of development of solute flux was evaluated by the clearance of 99mTc-labeled diethylenetriamine pentaacetate ( 99mTc-DTPA) from the lung, Afterwards, bronchoalveolar lavage (BAL) was performed to measure the concentration of albumin and determine the evidence of cell injury and inflammation in lung. BAL fluids were analyzed to determine several markers of cell injury and inflammation including total and differential cell counts, lactate dehydrogenase (LD), alkaline phosphatase (ALP), extracellular potassium (K+) and globulin (total protein minus albumin). 99mTc-DTPA clearance was significantly increased by exposure for 48 hours of hyperoxia. Albumin concentration ratio (BAL albumin concentration divided by serum albumin concentration) was increased sharply after 48 hr. Significant changes in WBC counts and differential counts were not found until 48 hr of hyperoxia. Elevated LD concentration was observed at 48 hr and thereafter, and ALP, K+, and globulin concentration ratio (BAL globulin /serum globulin) was significantly high only in group 4. Mortality was not observed until 72 hr when 3 of 8 rats were dead. It is concluded that significant 99mTc-DTPA clearance, and cellular and biochemical findings of BAL could not be observed until 48 hr in rats exposed to 100 % oxygen.
Subject(s)
Animals , Rats , Alkaline Phosphatase , Bronchoalveolar Lavage , Cell Count , Hyperoxia , Inflammation , L-Lactate Dehydrogenase , Lung , Mortality , Oxygen , Permeability , Potassium , Serum Albumin , Therapeutic IrrigationABSTRACT
Oxygen therapy is clear benefit in the treatment of tissue hypoxia, but high concentrations and long term exposures of oxygen carry the risks of detrimental physiologic changes and tissue damages. Tissue damages involve decreased surfactant production,alveolar edema, and alveolar hemorrhage. In spite of these damage, diagnosis of oxygen toxicity is difficult in many clinical settings. In this study, we measured lung compliance to evaluate the oxygen toxicity in 60 white rat of 100-150 g body weight Rats were divided into 6 groups. Group I was control graup, exposed to room air, group II -group V were exposed to 100% oxygen, group II for 24 hours, group IlI for 48 hous, group IV for 72 hours, and group V for 96 hours. Group VI was exposed to oxygen in serial as 30% oxygen for 24 hours, 60% oxygen for 24 hours and then 100% oxygen for 96 hours. After oxygen exposure we obseved changes of lung compliance and pathologic findings, compliance of group V was 15.94 mL/cmH2O significantly lower than that of eontrol group (p<0.05) and lung weight of group V was 2.16 g/100 g heavier than the other groups (p<0.05). Although we found oxygen tolerance was developed in group V, we could not differentiate the degree of pathologic damage cauesd from oxygen toxicity by pathologic findings. We concluded that the measurement of lung compliance is valuable in diagnosis of oxygen toxicity and thus in reducing lung damages.
Subject(s)
Animals , Rats , Hypoxia , Body Weight , Compliance , Diagnosis , Edema , Hemorrhage , Lung Compliance , Lung , OxygenABSTRACT
Oxygen therapy is clear benefit in the treatment of tissue hypoxia, but high concentrations and long term exposures of oxygen carry the risks of detrimental physiologic changes and tissue damages. Tissue damages involve decreased surfactant production,alveolar edema, and alveolar hemorrhage. In spite of these damage, diagnosis of oxygen toxicity is difficult in many clinical settings. In this study, we measured lung compliance to evaluate the oxygen toxicity in 60 white rat of 100-150 g body weight Rats were divided into 6 groups. Group I was control graup, exposed to room air, group II -group V were exposed to 100% oxygen, group II for 24 hours, group IlI for 48 hous, group IV for 72 hours, and group V for 96 hours. Group VI was exposed to oxygen in serial as 30% oxygen for 24 hours, 60% oxygen for 24 hours and then 100% oxygen for 96 hours. After oxygen exposure we obseved changes of lung compliance and pathologic findings, compliance of group V was 15.94 mL/cmH2O significantly lower than that of eontrol group (p<0.05) and lung weight of group V was 2.16 g/100 g heavier than the other groups (p<0.05). Although we found oxygen tolerance was developed in group V, we could not differentiate the degree of pathologic damage cauesd from oxygen toxicity by pathologic findings. We concluded that the measurement of lung compliance is valuable in diagnosis of oxygen toxicity and thus in reducing lung damages.
Subject(s)
Animals , Rats , Hypoxia , Body Weight , Compliance , Diagnosis , Edema , Hemorrhage , Lung Compliance , Lung , OxygenABSTRACT
Since the widespread application of hyperbaric oxygenation in clinical medicine, the problems of oxygen toxicity have been attracting a deep interest from the researchers on hyperbaric medicine as a practical issue. Among extensive research trials, the study on the protective agents oxygen toxicity occupied one of the most challenging field. As the mechanisms of oxygen toxicity, the role of the oxygen free radicals produced by peroxidation process are strongly accepted by the leading researchers on oxygen toxicity, the probable protective effects of antioxidant against oxygen toxicity are sustaining a sufficient rational. Maltol(2-methyl-3-hydroxy-gamma-pyrone) which is known to be a component of Korean red ginseng has been reporting to have an antioxidant action. But, further study is needed to provide definite evidence for this compound to be an antioxidant, since the action was based on the results which were obtained under in vitro experiment. In this study, the author attempted to evaluate the effect of maltol as protective agent against oxygen toxicity through the observation of death rate, convulsion rate, time to convulsion and microscopic pathological changes in some organs of experimental rats exposed to various conditions. The findings observed are as follows: 1) The death rate, convulsion rate, time to convulsion, lung/weight ratio and microscopic pathological finding of lung were identified as reliable objective and quantitative indices for oxygen toxicity. 2) Maltol showed excellent protective effect against pulmonary oxygen toxicity as an antioxidant.
Subject(s)
Animals , Rats , Clinical Medicine , Free Radicals , Hyperbaric Oxygenation , Lung , Mortality , Oxygen , Panax , Protective Agents , SeizuresABSTRACT
To investigate the effect of hyperoxia on EKG findings and to evaluate the applicability of EKG as noninvasive monitoring index of oxygen toxicity, 38 rabbits were continuously exposed to 6 different conditions-3 hyperbaric oxygenations (HBO-2.5, 3.5 and 5ATA, 100% O2), normobaric oxygenation (NBO, 100% O2), hyperbaric aeration (HBA-5ATA, 21% O2) and normobaric aeration (NBA, 21% O2)-for 120 minutes and their EKG and time to dyspnea and convulsion were recorded. Dyspnea and death were observed in exposure conditions of HBO-3.5 and HBO-5 (Positive rate of dyspnea; 10%, 100%, death; 10%, 25%, respectively) only, and convulsion in 4 oxygenation groups (NBO; 20%, HBO-2.5; 20%, HBO-3.5; 20%, HBO-5; 88%). Abnormal EKG findings included arrhythmia and ST-T changes and the incidences was increasing with doses(partial pressure of oxygen). In addition to EKG change, findings observed during exosure were dyspnea and convulsion in the order of appearence and when non specific ST-T change was accepted as positive (abnormal) finding, the frequency of abnormal EKG was statistically significant(p0.05). These results suggest that the effect of hyperoxia on heart is myocardial ischemia and arrhythmia, that oxygenation more than 3.5ATA causes myocardial damage in 120 minutes exposure, and that EKG is valuable as monitoring index of oxygen toxicity.
Subject(s)
Rabbits , Arrhythmias, Cardiac , Dyspnea , Electrocardiography , Heart , Hyperbaric Oxygenation , Hyperoxia , Incidence , Myocardial Ischemia , Oxygen , SeizuresABSTRACT
In vivo ethane production in rats was used as an index of oxygen toxicity. The rats were allocated to four exposure conditions; hyperbaric oxygenation (HBO=5 ATA, 100% O2), normobaric oxygenation (NBO=1 ATA, 100% O2), hyperbaric aeration (HBA=5 ATA, 21% O2) and normobaric aeration (NBA=1 ATA, 21% O2). After 120 minutes of exposure, the rats exposed to high concentration and/or high pressure oxygen exhaled significantly larger amounts of ethane than those exposed to NBA, and the differences in ethane production between any two groups were statistically significant (p<0.01). This finding supports the hypothesis that hypothesis that hyperoxia increase oxygen free-radicals and the radicals produce ethane as a result of lipid peroxidation. It is notable that the ethane exhalation level of the HBA group was significantly higher than that of the NBO group. This difference could not be accounted for by the alveolar oxygen partial pressure difference between the two groups.