摘要目的:探讨6%羟乙基淀粉130/0.4（HES）用于严重创伤骨科患者急性血液稀释后对蛋白的影响及发生机制。方法:选择2018年6至12月烟台市烟台山医院符合入选标准、择期行手术治疗的严重创伤骨科患者48例，随机数字表法分为两组（ n=24）：乳酸钠林格组（A组）和HES组（B组）。A组患者气管插管后经静脉以0.5 ml·kg -1·min -1的速率输注10%血容量的乳酸钠林格液行急性血液稀释。B组患者气管插管后经静脉以0.5 ml·kg -1·min -1的速率输注10%血容量的HES行急性血液稀释。急性血液稀释前即刻（T 0）、急性血液稀释后24 h（T 1）、48 h（T 2）测定总蛋白（TP）、血清白蛋白（HSA）、血浆循环内皮数量（CEC）、C反应蛋白（CRP）、血清肿瘤坏死因子α（TNF-α）、白细胞介素（IL）-10、IL-6。HES输入人体后与HSA结合，荧光光谱法分析HES和HSA的结合关系，进一步研究HES对HSA的影响。 结果:A组HSA、TP、CEC、TNF-ɑ、IL-6、IL-10、CRP在T 0时分别为（38±5）g/L、（66±5）g/L、（5.5±0.4）个/0.9 μl、（24±5）μg/L、（8.9±0.8）μg/L、（44±6）μg/L、（13.6±1.4）mg/L；在T 1时分别为（33±5）g/L、（60±6）g/L、（10.2±0.7）个/0.9 μl、（87±9）μg/L、（38.8±2.3）μg/L、（57±7）μg/L、（23.4±2.4）mg/L。B组HSA、TP、CEC、TNF-ɑ、IL-6、IL-10、CRP在T 0时分别为（38±4）g/L、（66±5）g/L、（5.4±0.6）个/0.9 μl、（24±6）μg/L、（9.1±0.9）μg/L、（45±6）μg/L、（13.4±1.8）mg/L；在T 1时分别为（35±5）g/L、（62±5）g/L、（7.4±0.6）个/0.9 μl、（70±8）μg/L、（29.5±3.1）μg/L、（72±6）μg/L、（19.7±2.2）mg/L。与T 0时比较，A组HSA、TP在T 1时降低（ P<0.05）；与T 0时比较，两组CEC在T 1时升高（ P<0.05）；与T 0相比，两组TNF-α、IL-6、IL-10、CRP在T 1和T 2时升高（ P<0.05）。与A组相比，B组CEC在T 1时降低（ P<0.05）；与A组相比，B组TNF-α、IL-6、CRP在T 1和T 2时降低（ P<0.05）；IL-10在T 1、T 2时升高（ P<0.05）。HES加入到HSA后，HSA的二级结构发生变化。随着HES浓度增加，HSA的荧光强度降低，HES诱发HSA荧光猝灭，HES与HSA的色氨酸（Trp）-214形成1∶1的结合物。 结论:HES减少严重创伤骨科患者术后低蛋白的发生，HES输入体内后与HSA的Trp-214结合形成1∶1复合物，体积增大利于HES的机械堵漏，同时与保护血管内皮细胞和抗炎作用有关。

abstractsObjective:To investigate the effect of 6% hydroxyethyl starch 130/0.4(HES) on protein in severe trauma orthopedic patients after acute hemodilution.Methods:Fourty-eight severe trauma patients who met the inclusion criteria were selected from June 2018 to December 2018 in Yantaishan Hospital, and were randomly divided into two groups ( n=24): group A and group B. Group A was ringer′s sodium lactate control group, and group B was HES treatment group. After the tracheal intubation, the patients of group A were infused with 10% blood volume of sodium lactate ringer at 0.5 ml·kg -1·min -1, and the patients in group B were infused with 10% blood volume of HES at 0.5 ml·kg -1·min -1. Total protein (TP), human serum albumin (HSA), numbers of circulating endothelium cells (CEC), C-reactive protein (CRP), and serum levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-10 and IL-6 were measured immediately after acute hemodilution (T 0), 24 hours (T 1) and 48 hours (T 2) after acute hemodilution. After infusion into human body, HES bond to HSA, and fluorescence spectroscopy was used to analyze the binding relationship between HES and HSA in order to further study the effects of HES on HSA. Results:The HSA, TP, CEC, TNF-α, IL-6, IL-10, CRP at T 0 of group A were (38±5) g/L, (66±5) g/L, (5.5±0.4)/0.9 μl, (24±5) μg/L, (8.9±0.8) μg/L, (44±6) μg/L, (13.6±1.4) mg/L; While at T 1 were (33±5) g/L, (60±6) g/L, (10.2±0.7)/0.9 μl, (87±9) μg/L, (38.8±2.3) μg/L, (57±7) μg/L, (23.4±2.4) mg/L. The HSA, TP, CEC, TNF-α, IL-6, IL-10, CRP at T 0 of group B were(38±4)g/L, (66±5) g/L, (5.4±0.6)/0.9 μl, (24±6) μg/L, (9.1±0.9) μg/L, (45±6) μg/L, (13.4±1.8) mg/L; While at T 1 were (35±5)g/L, (62±5)g/L, (7.4±0.6)/0.9 μl, (70±8) μg/L, (29.5±3.1) μg/L, (72±6) μg/L, (19.7±2.2) mg/L. HSA and TP decreased at T 1 in group A as compared with T 0 ( P<0.05), contrarily CEC increased significantly at T 1, TNF-ɑ, IL-6, IL-10 and CRP augmented at T 1 and T 2 in two groups ( P<0.05). In comparison with the patients of group A, CEC decreased significantly at T 1 ( P<0.05). TNF-ɑ, IL-6, CRP reduced significantly at T 1 and T 2 ( P<0.05), but IL-10 increased at T 1 and T 2 in group B ( P<0.05). The secondary structure of HSA changed after HES was added in the HES solution. The fluorescence intensity of HSA decreased with the increase of HES concentration,which suggested that HES induced HSA fluorescence quenching. HES could bind to Trp-214 residue in HSA at a molecular ration of 1∶1. Conclusions:6% HES reduces the occurrence of low protein level in severe trauma patients after operation. HES could bind to Trp-214 amino acid residue in HSA and form the complex at a molecular ratio of 1∶1. The formation of HES-HSA complex increases the volume of HES, avoids the vascular leakage, protects the vascular endothelial cells, and induces anti-inflammatory immunity in the patients with capillary syndrome.