Interrogating the pathophysiology of decompression sickness through the skin
Abstract
Approved for Public Release Current strategies to mitigate the risk of decompression sickness (DCS) (i.e., adherence to the U.S. Navy Dive Tables) hinder the operational capabilities by limiting dive depths and bottom times. Improved safety is currently achieved by following stringent decompression schedules and use of alternative breathing gases either during the dive or during decompression. However, emerging hypotheses highlight that DCS is a complex pathophysiological process characterized by oxidative stress, inflammation, and vascular injury/dysfunction indicating potential for novel countermeasures to be identified and developed. The overall objective of this three-year project is to interrogate cutaneous microvascular function and sweat- and blood-borne microparticles as indices of in vivo decompression stress in humans. Furthermore, we will investigate the role of oxygen breathing during decompression and the independent and combined effects of oxidative stress and/or inflammation on post-dive cutaneous microvascular function. We will address the following Aims: 1) determine the role of decompression mode on cutaneous microvascular function following a provocative dive, 2) identify the contributions of oxidative stress and inflammation on cutaneous microvascular function and the modifying effects of decompression mode selection, 3) examine the relation between sweat and blood-borne pro-inflammatory microparticles, and alterations in cutaneous microvascular function, and 4) examine the role of non-steroidal anti-inflammatory medication, antioxidant supplementation (ascorbic acid [Vitamin C]), and combination medication/supplementation on post-dive sweat and blood-borne pro-inflammatory microparticles, and alterations in cutaneous microvascular function. To do so, subjects will complete simulated, dry dives. In all simulated dives, the chamber will be pressurized to 100 fsw for a bottom time of 60 minutes. In the first study addressing Aims 1-3, subjects will complete decompression utilizing: 1) air only (81-minute stop at 20 fsw) or 2) oxygen only (33-minute stop at 20fsw). In the second study addressing Aim 4, subjects will complete three dives after the following interventions: 1) ascorbic acid supplementation, 2) non-steroidal anti-inflammatory medication, or 3) both ascorbic acid supplementation and non-steroidal anti-inflammatory medication. In both studies, blood samples will be obtained pre-dive, at depth, immediately post-dive, and 2 hours post-dive for microparticle analyses. Additionally, sweat samples will be collected pre- and 2 hours post-dive for microparticle analyses. Following decompression, assessment of cutaneous microvascular function utilizing intradermal microdialysis will be completed. The successful execution of these Aims will provide unique insights that will ultimately: (i) inform the mechanisms by which decompression mode modulates decompression stress (as observed via assessment of cutaneous microvascular function and microparticles), and (ii) identify targets (i.e., antioxidants and/or inflammatory blockade) for reducing decompression stress. The latter of which will advance the field by demonstrating improvements in functional outcomes (cutaneous microvascular function) and reductions in decompression-induced sequelae (pro-inflammatory microparticles). This will aid in the implementation of novel countermeasures to reduce the risk of DCS in Navy divers.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Apr 10, 2025
- Source ID
- N000142512259
Entities
People
- Hayden W Hess
Organizations
- Office of Naval Research
- Research Foundation for the State University of New York
- United States Navy