ArticleJournal of molecular histology2025
Combined skin injury model from airblast overpressure and seawater immersion in rats: establishment, characterization, and mechanistic insights.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
In maritime operations, individuals often face the threat of combined injury caused by airblast overpressure and seawater immersion. Airblast overpressure, induced by explosions, leads to significant internal damage despite the absence of visible open wounds. Seawater immersion exacerbates injuries due to its high osmolarity, microbial content, and thermal conductivity. Given the critical role of the skin as the body's largest organ, understanding its specific injuries in this scenario is imperative but currently underexplored. To bridge this gap, the study developed a novel rat skin combined injury model (RSCIM) in which rats were exposed to calibrated airblast overpressure followed by immediate seawater immersion. Physical simulations, histopathological examinations, and immunological assessments were used to confirm the model's accuracy. Specifically, finite element analysis reveals that the epidermal layer could effectively disperse and resist the immediate effects of overpressure. Histologically, the epidermal layer after combined injury maintained a continuous and complete structure. The collagen fibers of dermis were dispersed and broken. There were scattered capillaries, red blood cells and no skin appendages within the adipose layer. The muscle layer was manifested by deformation and breakage of muscle fibers. The fluorescence intensity of iNOS tended to decrease as the distance from the explosion source increased, which demonstrated significant inflammatory effects in the skin with combined injury. Furthermore, the transcriptome sequencing data revealed major physiological changes caused by combined injury, including inflammatory response, ion transport, biomechanical response, apoptosis, etc. Notably, S100A9 serves as a critical marker for combined injuries in RSCIM, but its expression characteristics and localization during tissue injury still need to be further explored. The model provides a robust foundation for exploring the combined injury mechanisms of airblast overpressure and seawater immersion and developing targeted therapeutic approaches.
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