Effect of angiotensin II on irradiation exacerbated decompression sickness.

In some complicated situations, decompression sickness (DCS) combined with other injuries, such as irradiation, will seriously endanger life safety. However, it is still unclear whether irradiation will increase the incidence of DCS. This study was designed to investigate the damage effects of irradiation on decompression injury and the underlying mechanism. Sprague-Dawley rats were exposed to irradiation followed by hyperbaric decompressing and the mortality and decompression symptoms were observed. Lung tissue and bronchoalveolar lavage fluid were collected to detect the lung lesion, inflammation response, activity of the angiotensin system, oxidative stress, and relative signal pathway by multiple methods, including Q-PCR, western blot, and ELISA. As a result, pre-exposure to radiation significantly exacerbated disease outcomes and lung lesions of DCS. Mechanically, the up-regulation of angiotensin-converting enzyme expression and angiotensin II levels was responsible for the exacerbated DCS and lung lesions caused by predisposing irradiation exposure. Oxidative stress and PI3K/AKT signal pathway activation in pulmonary tissue were enhanced after irradiation plus decompression treatment. In conclusion, our results suggested that irradiation could exacerbate lung injury and the outcomes of DCS by activating the angiotensin system, which included eliciting oxidative stress and activation of the PI3K/AKT signal pathway.

Microarray analysis and phenotypic response of Pseudomonas aeruginosa PAO1 under hyperbaric oxyhelium conditions.

Pseudomonas aeruginosa is an important opportunistic pathogen associated with multiple diseases including cystic fibrosis and nosocomial infections. Pseudomonas aeruginosa is also the microbe most often isolated from ear and skin infections in divers. Saturation divers often suffer from various skin and mucous disorders, of which P. aeruginosa infections are the most serious and frequent. Previous studies mainly focused on adaptive and regulatory mechanisms of P. aeruginosa virulence in inducing clinical acute and chronic infections under different environmental conditions. However, there are few studies describing the physiological adaptive and regulatory mechanisms of P. aeruginosa in inducing high infectivity in healthy divers under hyperbaric oxyhelium conditions and even fewer studies describing the overall influence of the hyperbaric oxyhelium environment on regulating mRNA and protein expression levels of P. aeruginosa. The present study used transcriptomic and virulence phenotype analysis to identify factors that allow P. aeruginosa to become established in a hyperbaric oxyhelium environment to facilitate infections in divers. Transcriptional profiling of P. aeruginosa grown under steady-state hyperbaric oxyhelium stress conditions showed an upregulation of genes associated with stress-sense/response, protein folding, transcriptional regulation, pili and flagellum metabolism, virulence adaptation, and membrane protein metabolism. Some of these genes (including several two-component systems not previously known to be influenced by hyperbaric oxyhelium) were differentially expressed by P. aeruginosa in response to 72 h of exposure to hyperbaric oxyhelium stress. Detection of the virulence phenotype confirmed the results of cDNA microarrays. Based on these results, we conclude that hyperbaric oxyhelium conditions affect PAO1 gene expression and upregulate the expression of most virulence genes. The data obtained in our study may provide new insight into the molecular mechanism of hyperbaric oxyhelium exposure against P. aeruginosa virulence adaptation.