Inhaled Hydrogen Sulfide Induces Suspended Animation, But Does Not Alter the Inflammatory Response After Blunt Chest Trauma
Inhaled Hydrogen Sulfide Induces Suspended Animation, But Does Not Alter the Inflammatory Response After Blunt Chest Trauma
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DOI：
10.1097/shk.0b013e31823f19a0
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发表时间：
2012-02
期刊：
影响因子：
3.1
通讯作者：
Daniel H. Seitz;J. Fröba;Ulrike Niesler;Annette Palmer;Heinrich A Veltkamp;Sonja T. Braumüller;F. Wagner;Katja Wagner;Stefan Bäder;U. Wachter;E. Calzia;P. Radermacher;M. Huber-Lang;Shaoxia Zhou;F. Gebhard;M. Knöferl
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文献类型：
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作者：
Daniel H. Seitz;J. Fröba;Ulrike Niesler;Annette Palmer;Heinrich A Veltkamp;Sonja T. Braumüller;F. Wagner;Katja Wagner;Stefan Bäder;U. Wachter;E. Calzia;P. Radermacher;M. Huber-Lang;Shaoxia Zhou;F. Gebhard;M. Knöferl
钝性胸外伤后急性肺损伤和脓毒性并发症的治疗仍然是一个挑战。吸入硫化氢（H2S）可能导致类似冬眠的代谢状态，这是指全身炎症反应减弱。因此，我们验证了吸入h2s诱导的假死可以减轻肺挫伤后炎症的假设。雄性Sprague-Dawley大鼠遭受钝性胸部创伤（冲击波）或假手术，随后暴露于H2S （100 ppm）或对照气体中6小时。通过植入的发射器测量体温和活动。在创伤后6、24、48小时处死动物，测定支气管肺泡灌洗液（BAL）的细胞含量以及BAL、血浆和培养上清血中单个核细胞、库普弗细胞、脾巨噬细胞和脾细胞的细胞因子浓度。吸入硫化氢导致体温和活动显著降低。创伤后48小时，当动物接受H2S时，创伤诱导的肺泡巨噬细胞计数增加被消除，而创伤诱导的中性粒细胞计数增加没有改变。此外，H2S吸入部分减弱了Kupffer细胞和脾细胞的BAL和培养上清中介质的释放；它改变了血浆细胞因子浓度，但不影响创伤引起的单核细胞培养上清的变化。这些发现表明，吸入H2S诱导创伤后代谢消耗减少，部分减轻炎症。然而，与缺氧或病原体诱导的肺损伤相比，H2S治疗在钝性胸部创伤后似乎没有保护作用。
ABSTRACT The treatment of acute lung injury and septic complications after blunt chest trauma remains a challenge. Inhaled hydrogen sulfide (H2S) may cause a hibernation-like metabolic state, which refers to an attenuated systemic inflammatory response. Therefore, we tested the hypothesis that inhaled H2S–induced suspended animation may attenuate the inflammation after pulmonary contusion. Male Sprague-Dawley rats were subjected to blunt chest trauma (blast wave) or sham procedure and subsequently exposed to a continuous flow of H2S (100 ppm) or control gas for 6 h. Body temperature and activity were measured by an implanted transmitter. At 6, 24, or 48 h after trauma, animals were killed, and the cellular contents of bronchoalveolar lavage (BAL) as well as cytokine concentrations in BAL, plasma, and culture supernatants of blood mononuclear cells, Kupffer cells, splenic macrophages, and splenocytes were determined. Hydrogen sulfide inhalation caused a significant reduction in body temperature and activity. The trauma-induced increase in alveolar macrophage counts was abrogated 48 h after trauma when animals received H2S, whereas the trauma-induced increase in neutrophil counts was unaltered. Furthermore, H2S inhalation partially attenuated the mediator release in BAL and culture supernatants of Kupffer cells as well as splenic cells; it altered plasma cytokine concentrations but did not affect the trauma-induced changes in mononuclear cell culture supernatants. These findings indicate that inhaled H2S induced a reduced metabolic expenditure and partially attenuated inflammation after trauma. Nevertheless, in contrast to hypoxic- or pathogen-induced lung injury, H2S treatment appears to have no protective effect after blunt chest trauma.