ArticleJournal of applied physiology (Bethesda, Md. : 1985)2013
Microparticles generated by decompression stress cause central nervous system injury manifested as neurohypophysial terminal action potential broadening.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins-Toward a Targeted Use of Oxygen?International journal of molecular sciences · 2022Trial
- Inflammatory responses to acute carbon monoxide poisoning and the role of plasma gelsolin.Science advances · 2025Article
- Case report: Biphasic autonomic response in decompression sickness: HRV and sinoatrial findings.Frontiers in physiology · 2025Article
- Recombinant human plasma gelsolin suppresses persistent neuroinflammation and restores hippocampal neurogenesis in murine model of decompression sickness.Journal of neurophysiology · 2024Article
- Inert Gas Mild Pressure Action on Healthy Humans: The "IPA" Study.International journal of molecular sciences · 2024Article
- Influence of exposure duration on human pressure-induced inflammatory responses: Comparison between tunnel workers and underwater divers.Physiological reports · 2024Article
- Gene expression of Decompression Sickness-resistant rats through a miRnome/transcriptome crossed approach.Communications biology · 2024Article
- Elevations of Extracellular Vesicles and Inflammatory Biomarkers in Closed Circuit SCUBA Divers.International journal of molecular sciences · 2023Article
- Neuroinflammation with increased glymphatic flow in a murine model of decompression sickness.Journal of neurophysiology · 2023Article
- Astrocyte-derived microparticles initiate a neuroinflammatory cycle due to carbon monoxide poisoning.Brain, behavior, & immunity - health · 2021Article
- Plasma gelsolin modulates the production and fate of IL-1β-containing microparticles following high-pressure exposure and decompression.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Diets and Cellular-Derived Microparticles: Weighing a Plausible Link With Cerebral Small Vessel Disease.Frontiers in cardiovascular medicine · 2021Review
- Dietary Gluten and Neurodegeneration: A Case for Preclinical Studies.International journal of molecular sciences · 2020Review
- Microparticle and interleukin-1β production with human simulated compressed air diving.Scientific reports · 2019Article
- Microglial-derived microparticles mediate neuroinflammation after traumatic brain injury.Journal of neuroinflammation · 2017Article
- Neutrophils generate microparticles during exposure to inert gases due to cytoskeletal oxidative stress.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The study goal was to use membrane voltage changes during neurohypophysial action potential (AP) propagation as an index of nerve function to evaluate the role that circulating microparticles (MPs) play in causing central nervous system injury in response to decompression stress in a murine model. Mice studied 1 h following decompression from 790 kPa air pressure for 2 h exhibit a 45% broadening of the neurohypophysial AP. Broadening did not occur if mice were injected with the MP lytic agent polyethylene glycol telomere B immediately after decompression, were rendered thrombocytopenic, or were treated with an inhibitor of nitric oxide synthase-2 (iNOS) prior to decompression, or in knockout (KO) mice lacking myeloperoxidase or iNOS. If MPs were harvested from control (no decompression) mice and injected into naive mice, no AP broadening occurred, but AP broadening was observed with injections of equal numbers of MPs from either wild-type or iNOS KO mice subjected to decompression stress. Although not required for AP broadening, MPs from decompressed mice, but not control mice, exhibit NADPH oxidase activation. We conclude that inherent differences in MPs from decompressed mice, rather than elevated MPs numbers, mediate neurological injury and that a component of the perivascular response to MPs involves iNOS. Additional study is needed to determine the mechanism of AP broadening and also mechanisms for MP generation associated with exposure to elevated gas pressure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.