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dc.contributor.authorBrett, K.D.
dc.contributor.authorYang, M.
dc.contributor.authorThom, S.R.
dc.date.accessioned2019-09-26T19:38:38Z
dc.date.available2019-09-26T19:38:38Z
dc.date.issued2019
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85072283974&doi=10.1038%2fs41598-019-49924-1&partnerID=40&md5=a0066e812c60877ed2d109f9a62b071a
dc.identifier.urihttp://hdl.handle.net/10713/11023
dc.description.abstractProduction of blood-borne microparticles (MPs), 0.1–1 µm diameter vesicles, and interleukin (IL)-1β in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1β elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1β by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1β by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1β by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1β concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1β occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study.en_US
dc.description.sponsorshipTis project was supported by the Canadian Forces Surgeon General Health Research Program, Grant N00014-16-1-2868 from the Ofce of Naval Research and an unrestricted grant from the National Foundation of Emergency Medicine.en_US
dc.description.urihttps://doi.org/10.1038/s41598-019-49924-1en_US
dc.language.isoen-USen_US
dc.publisherNature Publishing Groupen_US
dc.relation.ispartofScientific reports
dc.subjectblood-borne microparticlesen_US
dc.subjecthigh gas pressureen_US
dc.subject.meshBarotrauma--physiopathologyen_US
dc.subject.meshDecompressionen_US
dc.titleMicroparticle and interleukin-1β production with human simulated compressed air divingen_US
dc.typeArticleen_US
dc.identifier.doi10.1038/s41598-019-49924-1
dc.identifier.pmid31527725


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