[abstract] DECOMPRESSION-INDUCED VASCULAR INJURIES ARE CAUSED BY MICROPARTICLES

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[abstract] DECOMPRESSION-INDUCED VASCULAR INJURIES ARE CAUSED BY MICROPARTICLES

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dc.contributor.author Thom, S
dc.contributor.author Yang, M
dc.contributor.author Milovanova, T
dc.date.accessioned 2011-05-09T17:55:27Z
dc.date.available 2011-05-09T17:55:27Z
dc.date.issued 2010
dc.identifier.citation Undersea and Hyperbaric Medical Society Annual Meeting, St Pete Beach, Florida, USA. Undersea and Hyperbaric Medicine 2010 en
dc.identifier.issn 1066-2936
dc.identifier.uri http://archive.rubicon-foundation.org/9246
dc.description Abstract of the Undersea and Hyperbaric Medical Society, Inc. Annual Scientific Meeting, St Pete Beach, Florida, USA. (http://www.uhms.org) en
dc.description.abstract Introduction: Bubbles are central to the etiology of decompression pathophysiology but responses that mediate tissue injury remain unclear. We hypothesize that circulating pro-inflammatory microparticles (MPs) generated by decompression/bubble stress are the proximal cause for vascular damage. Increased MPs are present in humans subjected to simulated dives. Our goal was to elucidate events leading to decompression-induced vascular injury and explore strategies for MPs abatement. Materials and Methods: Mice subjected for 2 hours to air pressure equivalent to 60, 121 or 224 feet of sea water (fsw) were sacrificed at 1 or 24 hours for analysis of blood-borne MPs, neutrophil activation, tissue vascular leakage, as well as perivascular neutrophils, myeloperoxidase and cleaved caspase 3 [apoptosis marker]. Blood and tissue responses were then assessed after intravenous injection with antibodies to annexin V or an FDA-approved surfactant. Results: Decompression following all profiles triggered elevations in MPs (e.g. Control 2,134+48/µl (mean, SE, n=7) vs. 81,438+446/µl (p<0.05, n=4) 24 hours post 224 fsw exposure). Vascular leakage occurs in brain, skeletal muscle, psoas, omentum and heart following decompression at 1 & 24 hours. Intravascular neutrophil activation occurs following decompression and platelet MPs are adherent to the cell surface. Mice rendered thrombocytopenic or injected with tirofiban to inhibit platelet adherence do not show neutrophil activation or tissue injuries. Those injected with anti-annexin V or surfactant exhibited significant reductions in MPs, neutrophil activation and all injury markers. Conclusion: We conclude that platelet-derived MPs cause intravascular neutrophil activation and that subsequent perivascular endothelial adherence mediates tissue injury. Reducing platelet adherence or circulating MPs titer abrogates neutrophil activation and secondary perivascular injuries. en
dc.format.extent 258 bytes
dc.format.mimetype text/plain
dc.language.iso en_US en
dc.publisher Undersea and Hyperbaric Medical Society en
dc.subject decompression en
dc.subject vascular injuries en
dc.subject microparticles en
dc.subject pathophysiology en
dc.subject mice en
dc.subject animals en
dc.title [abstract] DECOMPRESSION-INDUCED VASCULAR INJURIES ARE CAUSED BY MICROPARTICLES en
dc.type Article en

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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