Seitz Daniel H, Perl Mario, Liener Ulrich C, Tauchmann Björn, Braumüller Sonja T, Brückner Uwe B, Gebhard Florian, Knöferl Markus W
Department of Trauma Surgery, Hand, Plastic and Reconstructive Surgery and Division of Surgical Research, University of Ulm, Ulm, Germany.
J Trauma. 2011 Jan;70(1):189-96. doi: 10.1097/TA.0b013e3181d7693c.
Chest trauma frequently occurs in severely injured patients and is often associated with hemorrhagic shock. Immune dysfunction contributes to the adverse outcome of multiple injuries. The aims of this study were to establish a combined model of lung contusion and hemorrhage and to evaluate the cardiopulmonary and immunologic response.
Male mice were subjected to sham procedure, chest trauma, hemorrhage (35 mm Hg±5 mm Hg, 60 minutes), or the combination. Respiratory rate, heart rate, and blood pressure were monitored. Plasma, Kupffer cells, blood monocytes, splenocytes, and splenic macrophages were isolated after 20 hours. Tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, 10, 12, 18, and macrophage inflammatory protein-2 levels in plasma and culture supernatants were determined.
Heart rate and blood pressure dropped in all groups, and after chest trauma and the double hit, these values remained reduced until the end of observation. Blood pressure was lower after the double hit than after the single hits. Plasma and Kupffer cell TNF-α concentrations were increased after lung contusion but not further enhanced by subsequent hemorrhage. Peripheral blood mononuclear cell (PBMC) TNF-α and IL-6 release were suppressed after the combined insult. IL-18 concentrations were increased in PBMC supernatants after chest trauma and in splenic macrophage supernatants of all groups.
Although physiologic readouts were selectively altered in response to the single or double hits, the combination did not uniformly augment the changes in inflammation. Our results suggest that the leading insult regarding the immunologic response is lung contusion, supporting the concept that lung contusion represents an important prognostic factor in multiple injuries.
胸部创伤在重伤患者中经常发生，且常与失血性休克相关。免疫功能障碍会导致多发伤出现不良后果。本研究的目的是建立肺挫伤和出血的联合模型，并评估心肺和免疫反应。
对雄性小鼠进行假手术、胸部创伤、出血（35毫米汞柱±5毫米汞柱，60分钟）或联合损伤。监测呼吸频率、心率和血压。20小时后分离血浆、库普弗细胞、血液单核细胞、脾细胞和脾巨噬细胞。测定血浆和培养上清液中肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-6、10、12、18和巨噬细胞炎性蛋白-2的水平。
所有组的心率和血压均下降，胸部创伤和双重打击后，这些值在观察结束前一直降低。双重打击后的血压低于单次打击后。肺挫伤后血浆和库普弗细胞TNF-α浓度升高，但随后的出血并未使其进一步升高。联合损伤后外周血单核细胞（PBMC）TNF-α和IL-6的释放受到抑制。胸部创伤后PBMC上清液和所有组脾巨噬细胞上清液中的IL-18浓度升高。
尽管生理指标在单次或双重打击后有选择性改变，但联合损伤并未一致地加剧炎症变化。我们的结果表明，免疫反应的主要损伤是肺挫伤，支持肺挫伤是多发伤重要预后因素的观点。
