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In a prospective, double-blind, randomised placebocontrolled study, we tested the hypothesis that a new formulation consisting of wheat gliadin chemically combined with a vegetal (thus orally effective) preparation of superoxide dismutase (SOD) allows to prevent hyperbaric oxygen (HBO)-induced oxidative cell stress.Twenty healthy volunteers were exposed to 100% oxygen breathing at 2.5 ATA for a total of 60 min. DNA strand breaks (tail moments) were determined using the alkaline version of the comet assay. Whole blood concentrations of reduced (GSH) and oxidised (GSSG) glutathione and F 2 -isoprostanes, SOD, glutathione peroxidase (GPx) and catalase (Cat) activities and red cell malondialdehyde (MDA) content were determined.After HBO exposure the tail moment ðp ¼ 0:03Þ and isoprostane levels ðp ¼ 0:049Þ were significantly lower in the group that received the vegetal formulation. Neither SOD and Cat nor GSH and GSSG were significantly affected by this preparation or HBO exposure. By contrast, blood GPx activity, which tended to be lower in the SODgroup already before the HBO exposure ðp ¼ 0:076Þ; was significantly lower afterwards ðp ¼ 0:045Þ:We conclude that an orally effective SOD-wheat gliadin mixture is able to protect against DNA damage, which coincided with reduced blood isoprostane levels, and may therefore be used as an antioxidant.
Hyperbaric oxygen (HBO) therapy is increasingly being used in different areas of medical practice. While demonstrated to be effective in several settings, its mechanism of action is not well understood. In the present study, we determined the effects of HBO on wound epithelialization and neovascularization in an in vivo hairless mouse ear "impaired" wound model. To impair wound healing, macrophages were depleted by pretreatment with iota-carrageenan. Wound epithelialization and neovascularization were measured using intravital microscopy and computerized planimetry. Metalloproteinase-2 (MMP-2), MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and tumor necrosis factor-alpha (TNF-alpha) were measured on days 2 and 7 using immunohistochemistry. In nonimpaired healing wounds, the rate of epithelialization and neovascularization was significantly accelerated in the groups treated with HBO. Time to wound closure was significantly delayed in impaired compared with nonimpaired healing wounds and HBO treatment completely reversed this delay. Neither HBO treatment nor macrophage depletion caused significant alterations in MMP-2 expression in wounds. In contrast, TNF-alpha, MMP-9, and TIMP-1 were significantly up-regulated in the impaired healing group receiving HBO treatment. These results show that HBO therapy effectively reversed the negative effect exerted by macrophage reduction on wound epithelialization and neovascularization. This beneficial effect could be due to stimulation of TNF-alpha production and, to a lesser degree due to release of metalloproteinases.
The incidence and nature of cardiac arrhythmias during static apnea were studied by monitoring the electrocardiogram (ECG) and oxygen saturation (SaO(2)) of 16 recreational breath-hold divers. All subjects completed a maximal apnea with a mean (+/-SD) breath-hold duration of 281 (+/-73) s without clinical complications. Both heart rate (HR) and SaO(2) decreased significantly with breath-hold duration. The decline in SaO(2) was inversely related to the decline in HR (r = -0.55, P < 0.05). Cardiac arrhythmias (supraventricular and ventricular premature complexes, right bundle branch block) occurred in 12/16 (77%) subjects and were related to breath-hold duration. Subjects with atrial premature complexes (n = 9) had a reduced BMI (P = 0.016) and a higher decline of the terminal SaO(2) (P = 0.01). In conclusion, ectopic arrhythmias were common during maximal static apneas for training purposes. The results indicate that the occurrence of ectopic beats is associated with individual factors such as the tolerable SaO(2) decrease.
Competitive breath-hold divers (BHD) employ glossopharyngeal insufflation (GI) to increase intrapulmonary oxygen stores and prevent the lungs from dangerous compressions at great depths. Glossopharyngeal insufflation is associated with inflation of the lungs beyond total lung capacity (TLC). It is currently unknown whether GI transiently over-distends the lungs or adversely affects lung elastic properties in the long-term. Resting lung function, ventilatory drive, muscle strength, and lung compliance were measured in eight BHD who performed GI since 5.5 (range 2-6) years on average, eight scuba divers, and eight control subjects. In five BHD subsequent measures of static lung compliance (Cstat) were obtained after 1 and 3 min following GI. Breath-hold divers had higher than predicted ventilatory flows and volumes and did not differ from control groups with regard to gas transfer, inspiratory muscle strength, and lung compliance. A blunted response to CO2 was obtained in BHD as compared to control groups. Upon GI there was an increase in mean vital capacity (VCGI) by 1.75 +/- 0.85 (SD) L compared to baseline (p < 0.001). In five BHD Cstat raised from 3.7 (range 2.9-6.8) L/kPa at baseline to 8.1 (range 3.4-21.2) L/kPa after maximal GI and thereafter gradually decreased to 5.6 (range 3.3-8.1) L/kPa after 1 min and 4.2 (range 2.7-6.6) L/kPa after 3 min (p < 0.01). We conclude that in experienced BHD there is a transient alteration in lung elastic recoil. Resting lung function did not reveal a pattern indicative of altered lung ventilatory or muscle function.
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