Yang Ming, Bhopale Veena M, Thom Stephen R
Department of Emergency Medicine, University of Maryland, Baltimore, Maryland.
Department of Emergency Medicine, University of Maryland, Baltimore, Maryland
J Appl Physiol (1985). 2015 Jul 1;119(1):77-82. doi: 10.1152/japplphysiol.00183.2015. Epub 2015 May 14.
We hypothesized that pathological changes associated with elevations in annexin V-positive microparticles (MPs) following high-pressure exposures can be abrogated by ascorbic acid in a murine model. Mice exposed for 2 h to 790-kPa air and killed at 2 or 13 h postdecompression exhibited over threefold elevations in circulating MPs, as well as subgroups bearing Ly6G, CD41, Ter119, CD31, and CD142 surface proteins. There was evidence of significant neutrophil activation, platelet-neutrophil interactions, and vascular injury to brain, omentum, psoas, and skeletal muscles assessed as leakage of high-molecular-weight dextran. Prophylactic ascorbic acid (500 mg/kg ip) administration prevented all postdecompression neutrophil changes and vascular injuries. Ascorbic acid administration immediately after decompression abrogated most changes, but evidence of vascular leakage in the brain and skeletal muscle at 13 h postdecompression persisted. No significant elevations in these parameters occurred after injection of ascorbic acid alone. The findings support the idea that MP production occurring with exposures to elevated gas pressure is an oxidative stress response and that antioxidants may offer protection from pathological effects associated with decompression.
我们假设，在小鼠模型中，高压暴露后与膜联蛋白V阳性微粒（MPs）升高相关的病理变化可被抗坏血酸消除。暴露于790 kPa空气2小时并在减压后2小时或13小时处死的小鼠，其循环MPs升高了三倍多，还有携带Ly6G、CD41、Ter119、CD31和CD142表面蛋白的亚群。有证据表明存在显著的中性粒细胞活化、血小板-中性粒细胞相互作用以及对脑、网膜、腰大肌和骨骼肌的血管损伤，通过高分子量葡聚糖渗漏来评估。预防性给予抗坏血酸（500 mg/kg腹腔注射）可预防减压后所有中性粒细胞变化和血管损伤。减压后立即给予抗坏血酸可消除大部分变化，但减压后13小时脑和骨骼肌中血管渗漏的证据仍然存在。单独注射抗坏血酸后这些参数没有显著升高。这些发现支持这样一种观点，即暴露于高压气体时发生的MP产生是一种氧化应激反应，抗氧化剂可能提供保护，使其免受与减压相关的病理影响。
