Skin lesions are visual clinical manifestations of decompression sickness (DCS). Comprehensive knowledge of skin lesions would give simple but strong clinical evidence to help diagnose DCS. The aim of this study was to systematically depict skin lesions and explore their pathophysiological basis in a swine DCS model. Thirteen Bama swine underwent simulated diving in a hyperbaric animal chamber with the profile of 40 msw-35 min exposure, followed by decompression in 11 min. After decompression, chronological changes in the appearance of skin lesions, skin ultrasound, temperature, tissue nitric oxide (NO) levels, and histopathology were studied. Meanwhile bubbles and central nervous system (CNS) function were monitored. All animals developed skin lesions and two died abruptly possibly due to cardiopulmonary failure. A staging approach was developed to divide the appearance into six consecutive stages, which could help diagnosing the progress of skin lesions. Bubbles were only seen in right but not left heart chambers. There were strong correlations between bubble load, lesion area, latency to lesion appearance and existence of cutaneous lesions (P = 0.007, P = 0.002, P = 0.004, respectively). Even though local skin temperature did not change significantly, skin thickness increased, NO elevated and histological changes were observed. Increased vessel echo-reflectors in lesion areas were detected ultrasonically. No CNS dysfunction was detected by treadmill walking and evoked potential. The present results suggest skin lesions mainly result from local bubbles and not CNS injuries or arterial bubbles.

Decompression sickness (DCS) occurs when ambient pressure is severely reduced during diving and aviation. Hyperbaric oxygen (HBO) pretreatment has been shown to exert beneficial effects on DCS in rats via heat-shock proteins (HSPs). We hypothesized that HBO pretreatment will also reduce DCS via HSPs in swine models. In the first part of our investigation, six swine were subjected to a session of HBO treatment. HSP32, 60, 70 and 90 were detected, before and at 6, 12, 18, 24 and 30 h following exposure in lymphocytes. In the second part of our investigation, another 10 swine were randomly assigned into two groups (five per group). All swine were subjected to two simulated air dives in a hyperbaric chamber with an interval of 7 days. Eighteen hours before each dive, the swine were pretreated with HBO or air: the first group received air pretreatment prior to the first dive and HBO pretreatment prior to the second; the second group were pretreated with HBO first and then air. Bubble loads, skin lesions, inflammation and endothelial markers were detected after each dive. In lymphocytes, all HSPs increased significantly (<0.05), with the greatest expression appearing at 18 h for HSP32 and 70. HBO pretreatment significantly reduced all the determined changes compared with air pretreatment. The results demonstrate that a single exposure to HBO 18 h prior to diving effectively protects against DCS in the swine model, possibly via induction of HSPs.

Endothelial dysfunction has been considered as pivotal in the pathogenesis of decompression sickness (DCS) and contributes substantively to subsequent inflammatory responses. Escin is well known for its endothelial protection and anti-inflammatory properties, and its protection against DCS has been proved in a rat model. This study aimed to further investigate the protection of escin against DCS in swine. Sixteen swine were subjected to a two-stage experiment with an interval of 7 days. In each stage, 7 days before a simulated air dive, the swine were treated with escin or saline. The first group received a successive administration of escin for 7 days prior to the first dive and saline for 7 days prior to the second; the second group was treated with saline and then escin. After decompression, signs of DCS and circulating bubbles were monitored, and blood was sampled for platelet count and determination of inflammatory and endothelial related indices. The death rate of DCS was markedly decreased in swine treated with escin compared with that in animals treated with saline, though not statistically significant due to the limited number of animals. Escin had no effect on bubble load but significantly ameliorated platelet reduction and endothelial dysfunction, as well as oxidative and inflammatory responses. The results further suggest the beneficial effects of escin on DCS by its endothelia-protective properties, and escin has the potential to be a candidate drug for DCS prevention and treatment.

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