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J Appl Physiol (1985). 2015 Sep 1;119(5):427-34. doi: 10.1152/japplphysiol.00380.2015. Epub 2015 Jul 2.

Association of microparticles and neutrophil activation with decompression sickness.

Author information

1
Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland; sthom@smail.umaryland.edu.
2
Department of Diving and Hyperbaric Medicine, Prince of Wales Hospital, New South Wales, Australia;
3
Department of Hyperbaric Medicine, Fiona Stanley Hospital, Perth, Western Australia;
4
Department of Hyperbaric Medicine, University of California Los Angeles Medical Center, Los Angeles, California;
5
Department of Emergency Medicine, The Townsville Hospital and College of Marine and Environmental Sciences, James Cook University, Townsville, Queensland, Australia;
6
Sahlgrenska University Hospital/Omrade2, Gothenburg, Sweden;
7
Divers Alert Network, Durham, North Carolina;
8
Department of Integrative Physiology, University of Split School of Medicine, Soltanska, Split, Croatia;
9
Divers Alert Network Europe Foundation and Diving Safety Laboratory, Roseto, Italy;
10
Divers Alert Network Europe Foundation and Diving Safety Laboratory, Roseto, Italy; Environmental, Occupational, Ageing and Integrative Physiology Laboratory, Haute Ecole Paul-Henri Spaak, Brussels, Belgium;
11
Centre for Hyperbaric Oxygen Therapy, Military Hospital Brussels, Brussels, Belgium; and.
12
Department of Emergency Medicine, Pereleman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
13
Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland;

Abstract

Decompression sickness (DCS) is a systemic disorder, assumed due to gas bubbles, but additional factors are likely to play a role. Circulating microparticles (MPs)--vesicular structures with diameters of 0.1-1.0 μm--have been implicated, but data in human divers have been lacking. We hypothesized that the number of blood-borne, Annexin V-positive MPs and neutrophil activation, assessed as surface MPO staining, would differ between self-contained underwater breathing-apparatus divers suffering from DCS vs. asymptomatic divers. Blood was analyzed from 280 divers who had been exposed to maximum depths from 7 to 105 meters; 185 were control/asymptomatic divers, and 90 were diagnosed with DCS. Elevations of MPs and neutrophil activation occurred in all divers but normalized within 24 h in those who were asymptomatic. MPs, bearing the following proteins: CD66b, CD41, CD31, CD142, CD235, and von Willebrand factor, were between 2.4- and 11.7-fold higher in blood from divers with DCS vs. asymptomatic divers, matched for time of sample acquisition, maximum diving depth, and breathing gas. Multiple logistic regression analysis documented significant associations (P < 0.001) between DCS and MPs and for neutrophil MPO staining. Effect estimates were not altered by gender, body mass index, use of nonsteroidal anti-inflammatory agents, or emergency oxygen treatment and were modestly influenced by divers' age, choice of breathing gas during diving, maximum diving depth, and whether repetitive diving had been performed. There were no significant associations between DCS and number of MPs without surface proteins listed above. We conclude that MP production and neutrophil activation exhibit strong associations with DCS.

KEYWORDS:

CD14; CD235; CD41; decompression sickness; myeloperoxidase; platelet-endothelial cell-adhesion molecule; tissue factor; von Willebrand factor

PMID:
26139218
DOI:
10.1152/japplphysiol.00380.2015
[Indexed for MEDLINE]
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