Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cidal activities of 24-h exposures to 100% O2 and 95% O2 + 5% CO2 were assayed at 1 and 3 ATA. Studied were 21 yeasts isolated from humans: Candida albicans (8 strains), C. tropicalis (3 strains), C. krusei (3 strains), C. parapsilosis (2 strains), C. guilliermondii (2 strains), and one strain each of C. pseudotropicalis, C. stellatoidea, and Torulopsis sp. Generally, these were extremely sensitive to hyperbaric oxygen, although species and strain differences were observed. Indices of kill from 80-100 (total kill) characterized 17 of the 21 yeasts (81%). Hyperoxia (O2 +/- CO2 at 1 ATA) was not lethal. Deprivation of CO2 as a consequence of hyperbaric exposure to 100% O2 enhanced cidal activity for only 2 of 21 yeasts, whereas hyperbaric exposure to the mixture enhanced activity against four yeasts. Cidal activities were not significantly different for the remaining 15 yeasts. This response to deprivation of CO2 is different from that of bacteria, and manifests fundamental differences between procaryotic and eucaryotic cells.
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PMID:Quantitative cidal activity of hyperbaric oxygen for opportunistic yeast pathogens. 56 66

The effect of oxygen (O2) exposure on the ability of the isolated, perfused rat lung to clear serotonin (5-hydroxytryptamine, 5-HT) from the perfusate was evaluated in normal or vitamin E-deficient Sprague-Dawley rats. Rats were exposed to 100% O2 at 1 ATA for 4-48 h. Lungs were subsequently isolated, artificially ventilated, and perfused in a recirculating system with Krebs-Ringer bicarbonate solution, pH 7.4 containing 3% bovine serum albumin and 0.25 muM [14C] 5-HT. 5HT clearance was calculated from the disappearance rate of [ 14C] 5-HT from the perfusate. In normal rats exposed to 100% O2, there was a progressive reduction in the clearance of 5-HT with increasing duration of O2 exposure. Compared to lungs from air-exposed controls, clearance was depressed 20% (P less than 0.01) after 18 h, 22% (P less than 0.01) after 24 h, and 35% (P less than 0.001) after 48 h. With vitamin E-deficient rats, the reduction in 5-HT clearance occurred after a shorter exposure time and was of greater magnitude than in rats on a normal diet. Depression of 5HT clearance by the lungs is an early alteration of lung function fue to hyperoxia and is potentiated by vitamin E deficiency. The most likely mechanism for the depression of 5-HT clearance is interference with the transport properties of lung endothelium.
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PMID:Depression of serotonin clearance by rat lungs during oxygen exposure. 83 74

To study extension of O2 tolerance by interruption of hyperoxic exposure, as compared to previous studies of continuous oxygen exposure, five healthy volunteers were exposed to oxygen at 2 ATA on an intermittent schedule of 20 min breathing O2, alternating with 5 min on a normoxic N2-O2 mixture. The cycle was repeated until symptoms or signs of O2 toxicity caused cessation of the experiment. Tracheal irritation and burning on inspiration occurred after 6-9 "oxygen hours" of exposure and progressed to severe tracheobronchial burning sensation, chest pain, and dyspnea after 11-15 h of O2. Average duration of exposure was 13.7 O2 h, inducing a mean vital capacity decrease of 10.3%. The decrease began soon after onset of symptoms. With intermittent O2 administration, nearly a doubling of the average duration of actual oxygen breathing was required to induce marked vital capacity change (greater than 10%) as compared to the previous studies of continuous O2 exposure. The increased duration of tolerable O2 exposure in man resembles the extension of O2 tolerance known to occur in animals exposed to intermittent hyperoxia.
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PMID:Extension of pulmonary O2 tolerance in man at 2 ATA by intermittent O2 exposure. 86 21

Clearance of 5-hydroxytryptamine (5-HT) by the lungs of normal and vitamin E-deficient rats was evaluated following a 60-min exposure to 100% oxygen (O2) at 4 ATA (HBO). After exposure, lungs were isolated, ventilated, and perfused, with a recirculating system used for measurement of 5-HT clearance. Control lungs were obtained from rats exposed to air at 1 ATA. In control normal rats, fractional clearance of 5-HT was 0.78+/-0.03 (mean+/-SE). Following HBO 5-HT clearance was 0.55+/-0.04 (P less than 0.01). In control vitamin E-deficient rats. 5-HT clearance was 0.85+/-0.05 and was decreased to 0.46+/-0.03 (P less than 0.001) following HBO. To evaluate the effect of recovery time after HBO on 5-HT clearance, separate groups of rats were killed at varying intervals post-HBO. In normal rats, 5-HT clearance had returned to control levels by 3-4 after HBO; in vitamin E-deficient rats, clearance remained unchanged 4 h after HBO and was only 74% (P less than 0.001) of control values 24 h post-HBO. These results indicate that depression of pulmonary 5-HT clearance occurs in rats due to hyperoxia and is potentiated by vitamin E deficiency. This represents a reversible alteration of lung function which requires vitamin E for complete recovery.
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PMID:Effect of hyperbaric oxygen exposure on pulmonary clearance of 5-hydroxytryptamine. 89 79

Impedance plethysmography was used to measure resting cardiac stroke volume (SV) and thoracic conductive volume (TCV) in four divers at intervals during a prolonged dry saturation dive (17 days at 18.6 ATA and 7 days' decompression). Resting heart rate (HR), blood pressure (BP), and pulmonary minute ventilation (VE) were measured 4 times per day for the duration of the 30-day experiment. The vital capacity (VC) and its subdivisions IC and ERV were measured by spirometry every 3 days. In nonsmokers, VC fell significantly with time (r = 0.64), while VC in smokers increased nearly 400 ml during the first week at pressure before tending to fall with time. Compared to predive, the mean ERV was increased 629 ml at pressure, while VE and respiratory rate were not changed. The increased ERV did not persist postdive and was probably the result of the increased work of breathing a dense gas (4.1 g/liters). Residual volume (RV) measured by nitrogen dilution before and after the dive increased 38% and remained significantly increased (22%) even after one year in 4 divers. It is suggested that hyperoxia (0.3 ATA PO2) combined with increased gas flow resistance caused the VC to fall and RV to increase. The major cardiovascular findings were a transient bradycardia associated with increased stroke volume leading to a significant increase in resting cardiac output associated with an increased rate of rapid ventricular filling, TCV, and BP at depth. Lowering the ambient temperature for 3 days did not re-establish the bradycardia, suggesting that hyperbaric bradycardia is not due to a subtle cold stress.
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PMID:Hana Kai II: a 17-day dry saturation dive at 18.6 ATA. IV. Cardiopulmonary functions. 91 Mar 17

Cardiorespiratory responses of four men to submaximal and maximal cycling exercise were observed during 17 days at 18.6 ATA. Inspired gas at pressure consisted of hyperoxic (PO2 = 232 mmHg) and normoxic (PO2 = 159 mmHg) helium mixtures with relative gas densities of 3.8 and 2.8, respectively. The average of pre- and postdive VO2max (1 ATA air), which were not significantly different, was 3.10 liters - min-1. During 5 min of submaximal exercise at 50% of VO2max, no significant difference in work rate, VO2, VCO2, VE, respiratory rate, heart rate (HR), stroke volume, blood pressures, or rectal temperature was noted at 18.6 ATA compared to 1 ATA with either gas mixture. Submaximal HR tended to decrease by 5 to 10 beats - min-1 at pressure, and in hyperoxia the VO2/HR ratio was significantly higher. Maximal exercise was performed to exhaustion at work rates requiring about 120% of VO2max. Significant increased in VO2max of 0.10 liter - min-1 (3%) and in endurance time of 2 min (48%) were found during hyperoxic gas breathing, whereas normoxic values at 18.6 ATA were similar to those at 1 ATA. Significant reductions in maximal HR of 8 beats - min-1 (4%) were observed with both gas mixtures at pressure, and VE was significantly decreased by 36 liters - min-1 (26%) in hyperoxia and 29 liters - min-1 (21%) in normoxia. No change was found in the calculated cardiac output. Maximal voluntary ventilation, which was measured only for the hyperoxic gas, fell significantly by 80 liters - min-1 (40%). Results indicate that aerobic power and endurance performance were affected by oxygen pressure. Normoxic work capacity, however, was not decreased at 18.6 ATA, despite marked reductions in HR and VE.
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PMID:Hana kai ii: a 17-day dry saturation dive at 18.6 ATA. V. Maximal oxygen uptake. 91 Mar 18

The influence of hypoxic acclimatization at altitudes of 0, 5,000, or 15,000 ft on the relative susceptibility to acute oxygen poisoning was determined in 288 adult female mice. After acclimatization periods of 1, 2, 4, or 8 wk, the mice were exposed to oxygen at high pressures (OHP) of 4, 6, or 9 ATA and the times to convulsion and death recorded. A factorial analysis of variance indicated that altitude and OHP level had inverse, log-linear effects on both parameters. The duration of acclimatization progressively decreased the time to death. The onset of convulsions and death was independent of body weight. There were significant interactions on the measured parameters between various combinations of altitude, OHP level, and duration of acclimatization. While alterations in the metabolism of gamma-aminobutyric acid and high-energy compounds are common to both hypoxia and hyperoxia, the most plausible explanation of the results relates to the decrease in buffer base induced by hypoxic acclimatization which might have caused CO2 potentiation of OHP symptoms.
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PMID:Relative susceptibility of altitude-acclimatized mice to acute oxygen toxicity. 112 Jul 52

Exposure to hyperoxia, especially under hyperbaric conditions, causes an enhanced oxidative stress particularly in lung tissue. To test the potential hazardous effect of either a single or repeated hyperbaric oxygen treatment (HBO) on the cellular defence system the glutathione status of lung tissue from rats exposed to HBO was investigated. When daily exposed to 2.5 ATA of > 95% O2 for 90 min over 8 or 14 days the content of reduced glutathione in lung tissue (GSH) increased by 16-19%. Oxidized glutathione (GSSG) tended to increase after 8 days and was 56% higher after 14 days. While the GSSG/GSH ratio was unchanged after 8 days, it increased by 39% after 14 days. Thus, the GSH increase after 8 days can be understood as a adaptive process to protect the lung from oxidative stress. The distinct increment of the cellular GSSG that lead to an increase of the GSSG/GSH ratio after 14 days reflects a situation, in which the cellular defence system is overwhelmed by oxidative stress. The additional pretreatment with perfluorochemicals in a dose of 2g/kg every second day aggravated the observed changes (GSH +39-19%, GSSG +118%). In a second experiment rats were exposed to a single session with 7 ATA of O2 for 60 min. GSH in the lungs increased for 40%, it was not elevated by PFC. However, GSSG increased to a much higher degree in untreated as well as in PFC-treated animals (+240%, +163%), elevating the ratio GSSG/GSH markedly (+145%, +176%). Allopurinol given as radical scavenger in a dose of 50 mg/kg was able to suppress the increased oxidative stress widely. Thus adaptive and overloading processes are involved under the treatment with increased oxygen pressures. As the administration of PFC aggravates the observed changes, a still increased blood oxygen offer must be considered as the causative agent. A radical scavenger is capable to suppress the increased oxidative stress widely.
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PMID:Effect of hyperbaric oxygen treatment and perfluorochemical administration on glutathione status of the lung. 128 20

Peripheral-type benzodiazepine Receptors (PBR) in the kidney and Central-type Benzodiazepine Receptors (CBR) in the cerebral cortex were not affected in rats exposed to chronic hyperoxia (85% O2, ATA, 6 days). Nevertheless, cortical CBR showed a significant decrease (29%) after hyperbaric hyperoxia (100% O2, 3.5 ATA, 2 h) in rats at a preconvulsive stage, with no concomitant alteration of kidney PBR. A similar down-regulation of striatal D2 dopamine receptors was noticed (27%)--after hyperbaric hyperoxia--without any modification of cortical PBR. On the contrary, an up regulation of liver PBR was obtained in the same conditions (20%). It is likely that receptors implicated in neurotransmission are particularly down regulated or altered under hyperbaric hyperoxia.
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PMID:Oxygen-induced modifications of benzodiazepine receptors and D2 dopamine receptors in the rat under hyperoxia. 166 66

To explore the role of glutathione in protecting rats from hyperbaric hyperoxia, we administered buthionine sulfoximine (BSO) to block gamma-glutamyl cysteine synthase activity and decrease tissue glutathione synthesis. We then exposed these animals and their vehicle-treated matched controls to 100% oxygen at 4 ATA or room air at 1 ATA. After BSO treatment, glutathione concentrations in air-exposed controls decreased 62% in lung, 76% in liver, 28% in brain, and 62% in plasma. Paradoxically, BSO-treated rats were protected from hyperbaric hyperoxia. The BSO-treated animals seized significantly later and had a markedly prolonged time of survival compared with the vehicle-treated controls. We conclude that BSO treatment protects rats from hyperbaric hyperoxia, despite its effects of lowering plasma and tissue glutathione concentrations. This protection may be related to a direct effect of the compound in decreasing free radical-mediated tissue injury, increasing tissue antioxidant defenses, or increasing seizure threshold.
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PMID:Protection from hyperbaric oxidant stress by administration of buthionine sulfoximine. 168 Aug 46


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