Microparticles generated by decompression stress cause central nervous system injury manifested as neurohypophysial terminal action potential broadening.
Microparticles generated by decompression stress cause central nervous system injury manifested as neurohypophysial terminal action potential broadening.
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DOI：
10.1152/japplphysiol.00745.2013
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发表时间：
2013-11
影响因子：
3.3
通讯作者：
Ming Yang;P. Kosterin;B. Salzberg;T. Milovanova;V. Bhopale;S. Thom
中科院分区：
文献类型：
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作者：
Ming Yang;P. Kosterin;B. Salzberg;T. Milovanova;V. Bhopale;S. Thom
本研究的目的是使用神经垂体动作电位（AP）传播过程中的膜电压变化作为神经功能的指标，以评估循环微粒（MP）在小鼠模型中引起减压应激引起中枢神经系统损伤中的作用。研究小鼠从790千帕的空气压力2小时减压后1小时表现出45%的神经垂体AP增宽。如果小鼠在减压后立即注射MP裂解剂聚乙二醇端粒B，使其出现血小板减少，或在减压前用一氧化氮合酶-2（iNOS）抑制剂治疗，或在缺乏髓过氧化物酶或iNOS的敲除（KO）小鼠中，则不会发生增宽。如果从对照（无减压）小鼠中收获MP并注射到幼稚小鼠中，则没有发生AP增宽，但在注射来自经受减压应激的野生型或iNOS KO小鼠的相等数量的MP时观察到AP增宽。虽然不需要AP加宽，MP从减压小鼠，而不是对照小鼠，表现出NADPH氧化酶激活。我们的结论是，固有的差异，从减压小鼠的MP，而不是升高的MP数量，介导神经损伤和血管周围的MP反应的一个组成部分涉及iNOS。需要进一步的研究来确定AP增宽的机制以及与暴露于升高的气体压力相关的MP产生的机制。
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.