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Bubble formation and platelet activation are major factors contributing to decompression sickness. We hypothesized that pretreatment with hyperbaric oxygen immediately before a dive may reduce bubble formation and platelet activation in humans. Five healthy volunteer subjects (1 female and 4 males; age, 33.6±2.9 years; height, 170±3 cm; weight, 71±8 kg, body mass index, 24.5±22.0 kg/m 2 ) participated in this study with a 4-day protocol. On day 1, a multiplace hyperbaric chamber was used to compress all subjects with air to 4 atmosphere absolute (ATA) for 25 minutes; they were then decompressed to surface pressure at a rate of 10 m/min. Once surface pressure was reached, they were monitored with precordial ultrasonic Doppler at 20 min, 50 min and 80 min. Venous blood samples were obtained immediately before and after pressure exposure. On day 2, all subjects were compressed at 1.6 ATA for 45 min with 100% oxygen; they were then decompressed to surface pressure at a rate of 10 m/min. As soon as they reached surface pressure, they were immediately exposed to the same compression-decompression protocol as day 1; blood samples were taken after the second pressure exposure. Platelet activation was examined before and after exposure. On days 3 and 4, we inverted the protocol to minimize the influence of the first immersion on bubble formation. In comparison to the standard compression protocol, compression after hyperbaric oxygenation led to significantly reduced bubble numbers and platelet activation (11.4%±0.7% vs. 5.4%±0.5%, p<0.05). This study shows that hyperbaric oxygenation pretreatment significantly reduces decompression-induced bubble formation and platelet activation. Hyperbaric oxygenation pretreatment may reduce the risk of decompression sickness in at-risk activities.

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Effect of in-water oxygen prebreathing at different depths on decompression-induced bubble formation and platelet activation in scuba divers was evaluated. Six volunteers participated in four diving protocols, with 2 wk of recovery between dives. On dive 1, before diving, all divers breathed normally for 20 min at the surface of the sea (Air). On dive 2, before diving, all divers breathed 100% oxygen for 20 min at the surface of the sea [normobaric oxygenation (NBO)]. On dive 3, before diving, all divers breathed 100% O2 for 20 min at 6 m of seawater [msw; hyperbaric oxygenation (HBO) 1.6 atmospheres absolute (ATA)]. On dive 4, before diving, all divers breathed 100% O2 for 20 min at 12 msw (HBO 2.2 ATA). Then they dove to 30 msw (4 ATA) for 20 min breathing air from scuba. After each dive, blood samples were collected as soon as the divers surfaced. Bubbles were measured at 20 and 50 min after decompression and converted to bubble count estimate (BCE) and numeric bubble grade (NBG). BCE and NBG were significantly lower in NBO than in Air [0.142+/-0.034 vs. 0.191+/-0.066 (P<0.05) and 1.61+/-0.25 vs. 1.89+/-0.31 (P<0.05), respectively] at 20 min, but not at 50 min. HBO at 1.6 ATA and 2.2 ATA has a similar significant effect of reducing BCE and NBG. BCE was 0.067+/-0.026 and 0.040+/-0.018 at 20 min and 0.030+/-0.022 and 0.020+/-0.020 at 50 min. NBG was 1.11+/-0.17 and 0.92+/-0.16 at 20 min and 0.83+/-0.18 and 0.75+/-0.16 at 50 min. Prebreathing NBO and HBO significantly alleviated decompression-induced platelet activation. Activation of CD62p was 3.0+/-0.4, 13.5+/-1.3, 10.7+/-0.9, 4.5+/-0.7, and 7.6+/-0.8% for baseline, Air, NBO, HBO at 1.6 ATA, and HBO at 2.2 ATA, respectively. The data show that prebreathing oxygen, more effective with HBO than NBO, decreases air bubbles and platelet activation and, therefore, may be beneficial in reducing the development of decompression sickness.

Hyperthermia produces regression of human cancer. Because hyperthermia has produced only limited results, attention has focused on searching for substances able to sensitize tumour cells to the effects of hyperthermia. The flavonoid quercetin has been reported to be a hyperthermic sensitizer in ovarian and uterine cervical tumours and in leukaemia. Quercetin and tamoxifen inhibit melanoma cell growth. We therefore investigated whether quercetin and tamoxifen can sensitize M10, M14 and MNT1 human melanoma cells to hyperthermia. We observed that both quercetin and tamoxifen synergize with hyperthermia (42.5 degrees C) in reducing the clonogenic activity of M14 and MNT1 and in inducing apoptotic cell death in all three cell lines. As revealed by flow cytometric and Northern blot analyses, quercetin and tamoxifen reduced heat shock protein-70 expression at both protein and mRNA levels. Our results suggest that quercetin and tamoxifen can be usefully combined with hyperthermia in the therapy of recurrent and/or metastatic melanoma.