Association of microparticles and neutrophil activation with decompression sickness

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.

Vascular dysfunction following breath-hold diving

“…During an actual breath-hold dive, divers are exposed to hyperoxia, hyperbaric conditions, cold ambient temperatures, physical exercise, dehydration, and psychological stress. All of these factors are present in SCUBA diving and they increase MP production and platelet and neutrophil activation (Thom et al 2013(Thom et al , 2015. In our breath-hold divers, although there was a difference in predive MP levels between the two protocols, both of them increased the absolute number of circulating MPs post-dive.…”

“…All divers took part in two separate diving protocols and they were randomly assigned to start with one of the diving protocols (five of them starting with protocol 1 and the other six with protocol 2). The two protocols were separated by 2 days where no diving was allowed (Thom et al 2015). After surfacing, bubble grades were assessed (see "Transthoracic echocardiography" below) and measurements of MPs and FMD were repeated.…”

“…In SCUBA, although the role of VGE in the genesis of DCS could not be ruled out, it is also not the only cause, which is evidenced by the fact that only 0.01% of divers develop DCS (Cialoni et al 2017). Other factors like vascular dysfunction, microparticles (MPs), and neutrophil activation have been identified as potential contributors (Thom et al 2013(Thom et al , 2015.…”

Time Course of Endothelial Dysfunction Induced by Decompression Bubbles in Rats

“…Several drugs were confirmed to be preventive to DCS partially through their endothelial-protective properties(Møllerløkken et al, 2006; Ni et al, 2011; Zhang et al, 2014, 2016a; Blatteau et al, 2015). It is now widely accepted that endothelial injury plays a significant role in the progress of DCS (Levett and Millar, 2008; Brubakk and Mollerlokken, 2009; Klinger et al, 2011; Vann et al, 2011; Thom et al, 2015). …”

Evidence for the infiltration of gas bubbles into the arterial circulation and neuronal injury following “yo-yo” dives in pigs

“…present study to find a direct correlation between symptoms of neurologic DCI and the incidence of injured neurons in the spinal cord. In the context of diving and DCI, such neuronal damage could be induced by ischemic events caused directly by gas bubbles that physically obstruct blood flow (22) or, indirectly, by activation of the immune system induced by gas bubbles inside blood vessels (9,10,16,22). The present study may also demonstrate that even though gas bubbles are necessary to induce DCI (22), the existence of bubbles per se is not sufficient to produce symptoms of DCI, including neuronal damage.…”