Microparticle enlargement is a key point of vascular injury caused by decompression stress

Objective Studies in a mouse model have shown that decompression stress increases the number of circulating microparticles (MPs), which precipitate neutrophil activation and vascular damage. Our objective was to discern whether their size was a strong contributor to pathophysiological changes caused by decompression stress. Methods MPs were isolated from mice subjected to 790 kPa air pressure for 2 hours. MPs size was measured by a multi‐photon microscope. MPs were injected into naïve mice via tail vein. Vascular injury was documented as elevations of vascular permeability and cleaved caspase 3. Results In control animals, 0.6±0.1 % of annexin V positive particles had diameters > 2.0 μm, while in 2 hours post‐decompression group this fraction increased to 9.8±1.8 % (p<0.05, n=5) and in 24 hours group 14.6±4.9 % (p<0.05, n=3). When 2 hours post‐decompression MPs samples were hydrostatically recompressed at 790 kPa pressure for 1 hour, the fraction of diameters > 2.0 μm was significantly reduced compared to without hydrostatic recompression group (p<0.05, n=5). When MPs with or without recompression were injected into naïve mice, both neutrophil activation and vascular damage were much less in those injected with recompression MPs. Conclusion we conclude that enlargement of annexin V positive microparticles plays an important role in tissue injury caused by decompression stress. This work was supported by a grant from the U.S. Office of Naval Research.