*Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School and Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria; †Defence Research and Development Canada, Toronto Research Centre and ‡Departments of Surgery and Critical Care Medicine, St Michael's Hospital, University of Toronto, Toronto, Ontario, Canada; §Department of Surgery, Harborview Medical Center, University of Washington, Seattle, Washington; ∥Brain Injury Laboratory, Cara Phelan Centre for Trauma Research Keenan Research Centre, Li Ka Shing Knowledge Institute, St Michael's Hospital, University of Toronto, Toronto, Ontario, Canada; and ¶American College of Surgeons, Department of Surgery, University of California, Irvine, California.
Shock. 2013 Nov;40(5):366-74. doi: 10.1097/SHK.0000000000000038.
Activation of polymorphonuclear neutrophils (PMNs) is thought to contribute to traumatic brain injury (TBI). Since hypertonic fluids can inhibit PMN activation, we studied whether hypertonic fluid resuscitation can reduce excessive PMN activation in TBI patients.
Trauma patients with severe TBI were resuscitated with 250 mL of either 7.5% hypertonic saline (HS; n = 22), HS + 6% dextran-70 (HSD; n = 22), or 0.9% normal saline (NS; n = 39), and blood samples were collected on hospital admission and 12 and 24 h after resuscitation. Polymorphonuclear neutrophil activation (CD11b, CD62L, CD64) and degranulation (CD63, CD66b, CD35) markers and oxidative-burst activity, as well as spontaneous PMN apoptosis were measured by flow cytometry.
Relative to healthy controls, TBI patients showed increased PMN activation and decreased apoptosis of PMNs. In the HS group, but not in the HSD group, markers of PMN adhesion (CD11b, CD64) and degranulation (CD35, CD66b) were significantly lower than those in the NS group. These effects were particularly pronounced 12 h after resuscitation. Treatment with HS and HSD inhibited PMN oxidative burst responses compared with NS-treated patients. Hypertonic saline alone partially restored delayed PMN apoptosis. Despite these differences, the groups did not differ in clinical outcome parameters such as mortality and Extended Glasgow Outcome Scale.
This study demonstrates that prehospital resuscitation with HS can partially restore normal PMN activity and the apoptotic behavior of PMNs, whereas resuscitation with HSD was largely ineffective. Although the results are intriguing, additional research will be required to translate these effects of HS into treatment strategies that improve clinical outcome in TBI patients.
多形核白细胞（PMN）的激活被认为是导致创伤性脑损伤（TBI）的原因之一。由于高渗液可以抑制PMN 的激活，我们研究了高渗液复苏是否可以减少 TBI 患者过度的PMN 激活。
严重 TBI 的创伤患者接受 250mL 以下液体复苏：7.5%高渗盐水（HS；n=22）、HS+6%右旋糖酐-70（HSD；n=22）或 0.9%生理盐水（NS；n=39），并在入院时以及复苏后 12 和 24 小时采集血样。通过流式细胞术测量多形核粒细胞激活（CD11b、CD62L、CD64）和脱颗粒（CD63、CD66b、CD35）标志物以及氧化爆发活性，以及自发性PMN 凋亡。
与健康对照组相比，TBI 患者表现出 PMN 激活增加和PMN 凋亡减少。在 HS 组中，但在 HSD 组中，PMN 黏附（CD11b、CD64）和脱颗粒（CD35、CD66b）标志物显著低于 NS 组。这些影响在复苏后 12 小时尤为明显。与 NS 治疗的患者相比，HS 和 HSD 治疗抑制了 PMN 氧化爆发反应。单独使用 HS 部分恢复了PMN 凋亡延迟。尽管存在这些差异，但各组在死亡率和格拉斯哥预后评分等临床结局参数上没有差异。
本研究表明，院前 HS 复苏可以部分恢复正常的PMN 活性和PMN 的凋亡行为，而 HSD 复苏则基本无效。尽管这些结果令人关注，但需要进一步的研究将 HS 的这些作用转化为改善 TBI 患者临床结局的治疗策略。
