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Introduction: Heat shock proteins (HSPs) and nuclear factor-kappa B (NF-KB) have been established as important mediators in lung injury; however, their role in preventing pulmonary toxicity from hyperbaric oxygen (HBO) has not been evaluated. Methods: We aimed to study the effects of heat shock (HS) injury on hyperbaric hyperoxic lung injury (HHLI) in a rat model and identify a mechanism of protection by evaluating HSP 27 and HSP 70 mRNA and protein levels, NF-KB p65, lung injury and oxidative parameters. By varying the times between HS and exposure to HBO, the pathways of interaction between HSPs and NF-KB will be further clarified. Results: Our results showed that HS exposure increases the mRNA and protein levels of HSP 27 and HSP 70; HS induced 10-fold increases of HSP 27 (9.77 ± 0.60) and HSP 70 (10.33 ± 2.4) within the first 10 h compared to control animals. Lesion scores were higher for the first 16 h after HS, but decreased again after 31 h (N = 7 animals; 5 lesions scores). Protein nitration showed no significant differences between groups exposed to HS or HBO; similarly there was no difference with a combination of both treatments. Discussion: HBO appears to attenuate the HS response by HSP 27 and HSP 70. Histopathology results suggest that HS might mitigate pathology in animals exposed to HS and HBO. No significant effect of HS on HBO-induced HHLI was observed in animals treated with both HS and HBO. [ABSTRACT FROM AUTHOR]

Background: The fraction of nitric oxide in exhaled gas (FENO) is reduced by 30-70% after exposure to partial pressures of oxygen (Po2) of 200-240 kPa for 90 min. The purpose of this study was to partition FENO into its flow-independent alveolar and bronchial components. A reduced bronchial NO flux (JawNO) is associated with induced bronchoconstriction, while increased alveolar NO concentration (CANO) is associated with increased alveolar dead space. Methods: There were 12 patients undergoing hyperbaric oxygen (HBO) therapy for 90 min at a Po2 of 240 kPa and 20 healthy subjects exposed to normobaric hyperoxia (NBO) breathing 100% oxygen for 90 min who were compared to a control group of 6 subjects breathing ambient air. FENO was measured at flow rates from 30 to 250 ml ∙s-1 before and after the exposures and the Högman Märilainen algorithm was used to calculate JawNO and CANO. Results: FENO at an expiratory flow rate of 50 ml ∙s-1 was reduced from 17.6 ± 8.3 to 12.3 ± 6.3 ppb after HBO exposure and from 17.8 ± 6.2 to 13.3 ± 5.2 ppb after NBO exposure. There was a significant reduction in JawNO, but unchanged CANO. There were no changes in the control experiment. Discussion: The reduction in FENO after exposure to normobaric and hyperbaric hyperoxia appears to be predominantly an airway effect. An unchanged and low CANO indicate preserved integrity of the gas exchange units without increased alveolar dead space at rest. [ABSTRACT FROM AUTHOR]

Introduction: The use of hyperbaric oxygen (HBO) to expedite decompression from saturation has not been proven and may increase risk of toxicity to the pulmonary system. To evaluate any benefit of HBO during decompression, we used a 70-kg swine model of saturation and examined lung tissue by microarray analysis for evidence of RNA regulation. Methods: Unrestrained, non-sedated swine were compressed to 132 fsw (5 ATA) for 22 h to achieve saturation. Animals then underwent decompression on air (AirD) or HBO (HBOD) starting at 45 fsw (2.36 ATA). Animals were evaluated for Type I and Type II decompression sickness (DCS) for 24 h. Control (SHAM) animals were placed in the chamber for the same duration, but were not compressed. Animals were sacrificed 24 h after exposure and total RNA was isolated from lung samples for microarray hybridizations on the Affymetrix platform. Results: There was no evidence of Type I DCS or severe cardiopulmonary DCS in any of the animals; abnormal gaits were noted only in the HBOD group (4/9). Three genes (nidogen 2, calcitonin-like receptor, and pentaxin-related gene) were significantly up-regulated in both the AirD and HBOD groups compared to controls. Three other genes (TN3, platelet basic protein, and cytochrome P450) were significantly down-regulated in both groups. Conclusions: HBO during decompression from saturation did not reduce the incidence of DCS. Gene regulation was apparent and similar in both the AirD and HBOD groups, particularly in genes related to immune function and cell signaling. [ABSTRACT FROM AUTHOR]

The article reports on the results of the study "Echocardiography in military oxygen divers," by A. Boussuges and colleagues. A description of the experimental set-up and measurement method is given. The study noted a greater left ventricular (LV) mass in oxygen military divers. It concluded that the echocardiographic differences divers and controls could be attributed to the high level physical training undertaken by them.

The article discusses a study by researcher Sydney Do and colleagues that suggests the crop-growing system proposed for the Mars One spaceflight program would produce too much oxygen and poison human inhabitants of the planned Mars base.

Comments on several studies which focus on some of oxygen's toxic properties. Oxygen as a damaging radical; Support for the idea that oxidative stress plays a role in aging; Report by Rajindar S. Sohal and Sanjiv Agarwal in the December 6, 1994 issue of the `Proceedings of the National Academy of Sciences,' who correlate a housefly's lifetime accumulation of oxidant-induced DNA damage with lifespan.