From the Division of Trauma, Emergency Surgery and Surgical Critical Care (M.S., C.H.J., A.I., J.O.H., M.D., G.V.), Department of Surgery, Massachusetts GeneralHospital/Harvard Medical School, Boston, Massachusetts; Department of Surgery (G.J., I.H., H.B.A.), University of Michigan, Ann Arbor, Michigan; and Department of Surgery (P.I.J.), University of Texas Medical School, Houston, Texas; and Department of Anesthesia (M.S., L.S.R.), Center of Head and Orthopedics, and Capital Region Blood Bank (C.H.J., P.I.J.), Copenhagen University Hospital, Rigshospitalet, Denmark.
J Trauma Acute Care Surg. 2014 Jan;76(1):12-9; discussion 19-20. doi: 10.1097/TA.0b013e3182aaa675.
Traumatic brain injury (TBI) and hemorrhagic shock (HS) can be associated with coagulopathy and inflammation, but the mechanisms are poorly understood. We hypothesized that a combination of TBI and HS would disturb coagulation, damage the endothelium, and activate inflammatory and complement systems.
A total of 33 swine were allocated to either TBI + HS (n = 27, TBI and volume-controlled 40% blood loss) or controls (n = 6, anesthesia and instrumentation). TBI + HS animals were left hypotensive (mean arterial pressure, 30-35 mm Hg) for 2 hours. Blood samples were drawn at baseline, 3 minutes and 15 minutes after injury, as well as following 2 hours of hypotension. Markers of coagulation, anticoagulation, endothelial activation/glycocalyx shedding, inflammation, complement, and sympathoadrenal function were measured.
The TBI + HS group demonstrated an immediate (3 minutes after injury) activation of coagulation (prothrombin fragment 1 + 2, 289 ng/mL vs. 232 ng/mL, p = 0.03) and complement (C5a, 2.83 ng/mL vs. 2.05 ng/mL, p = 0.05). Shedding of the endothelial glycocalyx (syndecan 1) was evident 15 minutes after injury (851.0 ng/ml vs. 715.5 ng/ml, p = 0.03) while inflammation (tumor necrosis factor α [TNF-α], 81.1 pg/mL vs. 50.8 pg/mL, p = 0.03) and activation of the protein C system (activated protein C, 56.7 ng/mL vs. 26.1 ng/mL, p = 0.01) were evident following the 2-hour hypotension phase.
The combination of TBI and shock results in an immediate activation of coagulation and complement systems with subsequent endothelial shedding, protein C activation, and inflammation.
颅脑损伤（TBI）和出血性休克（HS）可导致凝血功能障碍和炎症，但机制尚不清楚。我们假设 TBI 和 HS 的联合作用会扰乱凝血、损伤内皮，并激活炎症和补体系统。
共 33 头猪被分配到 TBI + HS 组（n = 27，TBI 和容量控制的 40%失血）或对照组（n = 6，麻醉和仪器）。TBI + HS 动物的平均动脉压（MAP）保持在 30-35mmHg 低血压状态 2 小时。在损伤后 3 分钟和 15 分钟以及低血压 2 小时后采集血液样本。测量凝血、抗凝、内皮激活/糖萼脱落、炎症、补体和交感肾上腺功能的标志物。
TBI + HS 组在损伤后立即（3 分钟后）激活凝血（凝血酶原片段 1 + 2，289ng/mL 比 232ng/mL，p = 0.03）和补体（C5a，2.83ng/mL 比 2.05ng/mL，p = 0.05）。内皮糖萼脱落（syndecan 1）在损伤后 15 分钟明显（851.0ng/ml 比 715.5ng/ml，p = 0.03），而炎症（肿瘤坏死因子-α[TNF-α]，81.1pg/mL 比 50.8pg/mL，p = 0.03）和蛋白 C 系统的激活（活化蛋白 C，56.7ng/mL 比 26.1ng/mL，p = 0.01）在低血压 2 小时后明显。
TBI 和休克的联合作用会立即激活凝血和补体系统，随后出现内皮脱落、蛋白 C 激活和炎症。
