Department of Orthopaedics and Trauma Surgery, Aachen University Medical Center, Aachen, Germany.
Cytokine. 2013 Feb;61(2):585-90. doi: 10.1016/j.cyto.2012.10.022. Epub 2012 Nov 22.
The hemorrhagic shock (HS) model is commonly used to initiate a systemic post-traumatic inflammatory response. Numerous experimental protocols exist and it is unclear how differences in these models affect the immune response making it difficult to compare results between studies. The aim of this study was to compare the inflammatory response of different established protocols for volume-controlled shock in a murine model.
Male C57/BL6 mice 6-10 weeks and weighing 20-25 g were subjected to volume-controlled or pressure-controlled hemorrhagic shock. In the volume-controlled group 300 μl, 500 μl, or 700 μl blood was collected over 15 min and mean arterial pressure was continuously monitored during the period of shock. In the pressure-controlled hemorrhagic shock group, blood volume was depleted with a goal mean arterial pressure of 35 mmHg for 90 min. Following hemorrhage, mice from all groups were resuscitated with the extracted blood and an equal volume of lactated ringer solution. Six hours from the initiation of hemorrhagic shock, serum IL-6, KC, MCP-1 and MPO activity within the lung and liver tissue were assessed.
In the volume-controlled group, the mice were able to compensate the initial blood loss within 30 min. Approximately 800 μl of blood volume was removed to achieve a MAP of 35 mmHg (p<0.001). No difference in the pro-inflammatory cytokine (IL-6 and KC) profile was measured between the volume-controlled groups (300 μl, 500 μl, or 700 μl). The pressure-controlled group demonstrated significantly higher cytokine levels (IL-6 and KC) than all volume-controlled groups. Pulmonary MPO activity increased with the severity of the HS (p<0.05). This relationship could not be observed in the liver.
Volume-controlled hemorrhagic shock performed following current literature recommendations may be insufficient to produce a profound post-traumatic inflammatory response. A decrease in the MAP following blood withdrawal (300 μl, 500 μl or 700 μl) was usually compensated within 30 min. Pressure-controlled hemorrhagic shock is a more reliable for induction of a systemic inflammatory response.
失血性休克（HS）模型通常用于引发全身性创伤后炎症反应。目前存在许多实验方案，但尚不清楚这些模型之间的差异如何影响免疫反应，这使得难以比较研究结果。本研究旨在比较不同已建立的容量控制休克模型在小鼠模型中的炎症反应。
6-10 周龄、体重 20-25g 的雄性 C57/BL6 小鼠接受容量控制或压力控制失血性休克。在容量控制组中，在 15 分钟内采集 300 μl、500 μl 或 700 μl 血液，并且在休克期间连续监测平均动脉压。在压力控制失血性休克组中，以 35mmHg 的目标平均动脉压耗竭血液容量 90 分钟。出血后，所有组的小鼠均通过提取的血液和等体积的乳酸林格溶液进行复苏。从失血性休克开始 6 小时后，评估血清 IL-6、KC、MCP-1 和肺和肝组织中的 MPO 活性。
在容量控制组中，小鼠能够在 30 分钟内补偿初始失血。大约 800 μl 的血液量被去除以达到 35mmHg 的 MAP（p<0.001）。在容量控制组之间（300 μl、500 μl 或 700 μl），没有测量到促炎细胞因子（IL-6 和 KC）谱的差异。压力控制组显示出比所有容量控制组更高的细胞因子水平（IL-6 和 KC）。HS 的严重程度与肺 MPO 活性增加相关（p<0.05）。这种关系在肝脏中无法观察到。
按照当前文献建议进行的容量控制失血性休克可能不足以产生严重的创伤后炎症反应。在采血后（300 μl、500 μl 或 700 μl）MAP 下降通常在 30 分钟内得到补偿。压力控制失血性休克更可靠地诱导全身性炎症反应。
