[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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Title: [abstract] DECOMPRESSION-INDUCED VASCULAR INJURIES ARE CAUSED BY MICROPARTICLES
Author: Thom, S; Yang, M; Milovanova, T
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.
Description: Abstract of the Undersea and Hyperbaric Medical Society, Inc. Annual Scientific Meeting, St Pete Beach, Florida, USA. (http://www.uhms.org)
URI: http://archive.rubicon-foundation.org/9246
Date: 2010

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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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