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Ascorbic acid abrogates microparticle generation and vascular injuries associated with high-pressure exposure
Ming Yang1, Veena M Bhopale1, Stephen R Thom2
1Department of Emergency Medicine, University of Maryland, Baltimore, Maryland.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|May 16, 2015
Summary
High-pressure exposures increase microparticles (MPs) and cause vascular injury. Ascorbic acid (vitamin C) prevents these effects, suggesting MPs are an oxidative stress response.
Area of Science:
- Biomedical Science
- Physiology
- Toxicology
Background:
- High-pressure exposures can lead to pathological changes.
- Elevated circulating microparticles (MPs) are associated with these changes.
- Oxidative stress is implicated in decompression-related pathologies.
Purpose of the Study:
- To investigate the protective effects of ascorbic acid against pathological changes induced by high-pressure exposure.
- To determine if microparticle production is an oxidative stress response.
- To assess the efficacy of ascorbic acid administered before and after decompression.
Main Methods:
- Murine model exposed to 790-kPa air for 2 hours.
- Assessment of circulating MPs with specific surface protein markers (Ly6G, CD41, Ter119, CD31, CD142).
- Evaluation of neutrophil activation, platelet-neutrophil interactions, and vascular injury via dextran leakage.
Main Results:
- Decompression caused threefold elevations in circulating MPs and significant vascular injury in multiple organs.
- Prophylactic ascorbic acid (500 mg/kg) prevented all neutrophil changes and vascular injuries.
- Post-decompression ascorbic acid mitigated most, but not all, vascular leakage.
Conclusions:
- Microparticle production following high-pressure exposure is likely an oxidative stress response.
- Ascorbic acid demonstrates protective effects against decompression-induced pathology.
- Antioxidants may serve as a therapeutic strategy for decompression-related injuries.
