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ENGLISH ABSTRACT
创伤早期不同剂量氨甲环酸治疗急进高原兔创伤失血性休克的效果比较
刘圳
聂超
袁梨嘉
杨玲
蒋慧
钱程
蔡凌虎
张翼
刘明华
作者及单位信息
·
DOI： 10.3760/cma.j.cn501098-20240912-00558
Comparative efficacy of different doses of tranexamic acid for traumatic hemorrhagic shock in the early phase of trauma following acute exposure to high altitude in rabbits
Liu Zhen
Nie Chao
Yuan Lijia
Yang Ling
Jiang Hui
Qian Cheng
Cai Linghu
Zhang Yi
Liu Minghua
Authors Info & Affiliations
Liu Zhen
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Nie Chao
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Yuan Lijia
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Yang Ling
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Jiang Hui
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Qian Cheng
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Cai Linghu
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Zhang Yi
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
Liu Minghua
Emergency Department, First Affiliated Hospital of Army Medical University, Chongqing 400038, China
·
DOI： 10.3760/cma.j.cn501098-20240912-00558
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摘要

目的比较创伤早期不同剂量氨甲环酸（TXA）治疗急进高原兔创伤失血性休克（THS）的效果。

方法25只健康雄性新西兰兔按随机数字表法分为平原对照组（5只）和急进高原THS组（20只)，其中平原对照组全程不进行THS建模操作，急进高原THS组置于体积分数10%的低氧模拟仓内饲养3 d，即于仓内构建THS模型。根据急进高原THS建模后30 min静脉缓慢推注TXA剂量的不同，将急进高原THS组分为4个亚组：急进高原THS+0 mg/kg TXA组、急进高原THS+45 mg/kg TXA组、急进高原THS+90 mg/kg TXA组和急进高原THS+135 mg/kg TXA组，每组5只。分别在失血前、失血后30 min和失血后120 min记录兔的生命体征［平均动脉压（MAP）、心率、肛温］和血液样本中血细胞计数［红细胞计数（RBC）、血小板计数（PLT）］、凝血四项［纤维蛋白原（FIB）、D-二聚体、活化部分凝血活酶时间（APTT）、凝血酶原时间（PT）］、血栓弹力图参数［凝血反应时间（R值）、血凝块形成时间（K值）、血凝块最大强度（MA值）］、多配体蛋白聚糖-1（Syndecan-1）、炎症因子［白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）］和纤溶酶原激活物抑制剂-1（PAI-1）；THS后6 h，取兔的肺、回肠末端和肾等组织观察组织损伤情况，并检测肺组织湿/干重比（W/D）和总含水量（TLW）。

结果（1）生命体征：失血前，急进高原THS各组较平原对照组MAP、心率和肛温差异均无统计学意义（ P>0.05）；失血后30 min和120 min，急进高原THS各组较平原对照组MAP、心率和肛温均降低（ P<0.05）；急进高原THS各组间各时间点MAP、心率和肛温差异均无统计学意义（ P>0.05）。急进高原THS各组内MAP、心率及肛温在失血后30 min和120 min时较失血前均降低（ P<0.05），失血后120 min较失血后30 min均降低（ P<0.05）。（2）血细胞计数：失血前，急进高原THS各组较平原对照组RBC均增加（ P<0.05），PLT均减少（ P<0.05）。失血后30 min，急进高原THS各组较平原对照组RBC差异均无统计学意义（ P>0.05），PLT均降低（ P<0.05）。失血后120 min，急进高原THS各组较平原对照组RBC均降低（ P<0.05），急进高原THS各组间RBC差异均无统计学意义（ P>0.05）；急进高原THS+0 mg/kg TXA组较其余急进高原THS组PLT均减少（ P<0.05）；急进高原THS+45 mg/kg TXA组较急进高原THS+90 mg/kg TXA组和急进高原THS+135 mg/kg TXA组PLT均减少（ P<0.05），急进高原THS+90 mg/kg TXA组较急进高原THS+135 mg/kg TXA组PLT差异无统计学意义（ P>0.05）。（3）凝血四项检测：失血前，急进高原THS各组较平原对照组D-二聚体均增加（ P<0.05），FIB差异均无统计学意义（ P>0.05），APTT和PT均缩短（ P<0.05）；失血后30 min，急进高原THS各组较平原对照组D-二聚体均增加（ P<0.05），FIB均减少（ P<0.05），APTT和PT均延长（ P<0.05）。失血后120 min，急进高原THS+0 mg/kg TXA组较其余急进高原THS组D-二聚体均增加（ P<0.05），FIB均减少（ P<0.05），APTT和PT均延长（ P<0.05）；急进高原THS+45 mg/kg TXA组较急进高原THS+90 mg/kg TXA组和急进高原THS+135 mg/kg TXA组D-二聚体均增加（ P<0.05），FIB均减少（ P<0.05），APTT和PT均延长（ P<0.05）；急进高原THS+90 mg/kg TXA组较急进高原THS+135 mg/kg TXA组D-二聚体、FIB、APTT和PT差异均无统计学意义（ P>0.05）。（4）血栓弹力图参数：失血前，急进高原THS各组较平原对照组R值均缩短（ P<0.05），K值和MA值差异均无统计学意义（ P>0.05）；失血后30 min，急进高原THS各组较平原对照组R值和K值均缩短（ P<0.05），MA值差异均无统计学意义（ P>0.05）。失血后120 min，急进高原THS+0 mg/kg TXA组较其余各组R值和K值均延长（ P<0.05），MA值均降低（ P<0.05）；其余急进高原THS组较平原对照组R值和K值均缩短（ P<0.05），MA值均降低（ P<0.05）；急进高原THS+45 mg/kg TXA组较急进高原THS+90 mg/kg TXA组和急进高原THS+135 mg/kg TXA组R值和K值均降低（ P<0.05），MA值均降低（ P<0.05）；急进高原THS+90 mg/kg TXA组较急进高原THS+135 mg/kg TXA组R值、K值和MA值差异均无统计学意义（ P>0.05）。（5）Syndecan-1、炎症因子和PAI-1变化：失血前，急进高原THS各组较平原对照组Syndecan-1均增加（ P<0.05），IL-6、TNF-α和PAI-1差异均无统计学意义（ P>0.05）。失血后30 min，急进高原THS各组较平原对照组Syndecan-1、IL-6、TNF-α和PAI-1均增加（ P<0.05）。失血后120 min，急进高原THS各组较平原对照组Syndecan-1、IL-6、TNF-α和PAI-1均增加（ P<0.05）；急进高原THS+0 mg/kg TXA组较其余急进高原THS组Syndecan-1、IL-6、TNF-α和PAI-1均增加（ P<0.05）；急进高原THS+45 mg/kg TXA组较急进高原THS+90 mg/kg TXA组和急进高原THS+135 mg/kg TXA组Syndecan-1、IL-6和TNF-α均增加（ P<0.05），PAI-1差异均无统计学意义（ P>0.05）；急进高原THS+90 mg/kg TXA组较急进高原THS+135 mg/kg TXA组Syndecan-1、IL-6、TNF-α和PAI-1差异均无统计学意义（ P>0.05）。（6）组织损伤：THS 后6 h，急进高原THS+0 mg/kg TXA组肺间质显著增厚伴大量炎性细胞浸润，局部肠道纹状缘缺失伴细胞破裂并出现肾小体结构破坏明显伴局部细胞损伤坏死，其肺损伤评分、Chiu氏肠道评分和肾损伤评分较其余各组均增加（ P<0.05），其余各组肺、肠和肾脏组织损伤评分差异均无统计学意义（ P>0.05）。THS后6 h，急进高原THS+0 mg/kg TXA组较其余各组肺W/D和TLW均增加（ P<0.05）；急进高原THS+45 mg/kg TXA组较急进高原THS+90 mg/kg TXA组和急进高原THS+135 mg/kg TXA组肺W/D和TLW均增加（ P<0.05）；急进高原THS+90 mg/kg TXA组较急进高原THS+135 mg/kg TXA组肺W/D和TLW差异均无统计学意义（ P>0.05）。

结论兔急进高原3 d时，血液呈高凝状态伴随内皮细胞屏障受损；在急进高原THS 30 min时，单次静脉缓慢推注90 mg/kg和135 mg/kg剂量的TXA较45 mg/kg更能有效地改善兔的凝血纤溶功能、抑制炎症反应、缓解内皮细胞损伤及减少肺水肿发生风险。

高海拔;休克，创伤性;出血;氨甲环酸
ABSTRACT

ObjectiveTo compare the efficacy of different doses of tranexamic acid (TXA) for traumatic hemorrhagic shock (THS) in the early phase of trauma following acute exposure to high altitude in rabbits.

MethodsTwenty-five healthy male New Zealand rabbits were randomly divided into plain control group ( n=5) and acute high-altitude THS group ( n=20) according to the random number table method. The plain control group did not undergo THS modeling throughout the experiment while the acute high-altitude THS group was raised in a hypoxia simulation chamber with a volume fraction of 10% for 3 days to establish the THS model. Based on the different doses of TXA administered intravenously at 30 minutes after THS modeling, the acute high-altitude THS group was further divided into four subgroups: acute high-altitude THS+0 mg/kg TXA subgroup, acute high-altitude THS+45 mg/kg TXA subgroup, acute high-altitude THS+90 mg/kg TXA subgroup and acute high-altitude THS+135 mg/kg TXA subgroup, with 5 rabbits in each. The vital signs [mean arterial pressure (MAP), heart rate, rectal temperature] and blood cell counts [red blood cell count (RBC), platelet count (PLT)], 4 coagulation parameters [fibrinogen (FIB), D-dimer, activated partial thromboplastin time (APTT), prothrombin time (PT)], thromboelastography [clotting reaction time (R value), clot formation time (K value), maximum amplitude (MA value)], syndecan-1, inflammatory factors [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α)], and plasminogen activator inhibitor-1 (PAI-1) were recorded before blood loss, at 30 minutes and 120 minutes after blood loss. At 6 hours after THS, the lungs, terminal ileum, and kidneys of the rabbits were collected to observe tissue damage, and the wet/dry weight ratio (W/D) and total water content (TLW) of the lung tissue were measured.

Results(1) Vital signs: Before blood loss, there were no significant differences in MAP, heart rate, or rectal temperature between the acute high-altitude THS subgroups and the plain control group ( P>0.05). At 30 minutes and 120 minutes after blood loss, the acute high-altitude THS subgroups exhibited significantly lower MAP, heart rate, and rectal temperature compared to those in the plain control group ( P<0.05). No significant differences were observed in MAP, heart rate or rectal temperature among the acute high-altitude THS subgroups at any time point ( P>0.05). In the acute high-altitude THS subgroups, MAP, heart rate and rectal temperature were significantly decreased at 30 minutes and 120 minutes after blood loss compared to those before blood loss ( P<0.05); At 120 minutes after blood loss, these parameters were further significantly decreased compared to those at 30 minutes after blood loss ( P<0.05). (2) Blood cell counts: Before blood loss, the RBC count was significantly higher in the acute high-altitude THS subgroups compared to that in the plain control group ( P<0.05), while the PLT was significantly lower ( P<0.05). At 30 minutes after blood loss, there was no significant difference in RBC count between the acute high-altitude THS subgroups and the plain control group ( P>0.05), but the PLT remained significantly lower in the acute high-altitude THS subgroups ( P<0.05). At 120 minutes after blood loss, the RBC count was significantly lower in the acute high-altitude THS subgroups compared to that in the plain control group ( P<0.05), with no significant differences among the acute high-altitude THS subgroups ( P>0.05). The PLT count was significantly lower in the acute high-altitude THS+0 mg/kg TXA subgroup compared to the other subgroups ( P<0.05). The PLT count in the acute high-altitude THS+45 mg/kg TXA subgroup was significantly lower than those in the acute high-altitude THS+90 mg/kg TXA and acute high-altitude THS+135 mg/kg TXA subgroups ( P<0.05), with no significant differences between the latter two subgroups ( P>0.05). (3) Four Coagulation parameters: Before blood loss, D-dimer level was significantly higher in the acute high-altitude THS subgroups compared to that in the plain control group ( P<0.05), while no significant difference was observed in FIB ( P>0.05). APTT and PT were significantly shortened in the acute high-altitude THS subgroups ( P<0.05). At 30 minutes after blood loss, D-dimer level remained significantly higher in the acute high-altitude THS subgroups compared to that in the plain control group ( P<0.05), while FIB was significantly lower ( P<0.05), with significant increase of APTT and PT compared to those before blood loss ( P<0.05). At 120 minutes after blood loss, the acute high-altitude THS+0 mg/kg TXA subgroup exhibited significantly higher D-dimer level compared to the other subgroups ( P<0.05), with significantly lower FIB and higher APTT and PT ( P<0.05). The acute high-altitude THS+45 mg/kg TXA subgroup also showed significantly higher D-dimer level compared to those in the acute high-altitude THS+90 mg/kg TXA and acute high-altitude THS+135 mg/kg TXA subgroups ( P<0.05), with significantly lower FIB and increased APTT and PT ( P<0.05). No significant differences were observed in D-dimer, FIB, APTT or PT between the acute high-altitude THS+90 mg/kg TXA and acute high-altitude THS+135 mg/kg TXA subgroups ( P>0.05). (4) Thromboelastography parameters: Before blood loss, the R value was significantly shorter in the acute high-altitude THS subgroups compared to that in the plain control group ( P<0.05), while no significant differences were observed in K value or MA value ( P>0.05). At 30 minutes after blood loss, both R value and K value were significantly shorter in the acute high-altitude THS subgroups compared to those in the plain control group ( P<0.05), with no significant differences in MA value ( P>0.05). At 120 minutes after blood loss, the acute high-altitude THS+0 mg/kg TXA subgroup exhibited significantly increased R value and K value compared to those in the other subgroups ( P<0.05), while MA value was significantly decreased ( P<0.05). The remaining acute high-altitude THS subgroups showed significant decrease of R value and K value compared to those in the plain control group ( P<0.05), while MA value was significantly lower ( P<0.05). The acute high-altitude THS+45 mg/kg TXA subgroup exhibited significantly lower R value and K value compared to those in the acute high-altitude THS+90 mg/kg TXA and acute high-altitude THS+135 mg/kg TXA subgroups ( P<0.05), with no significant differences in R value, K value and MA value between the later two groups ( P<0.05). (5) Changes in Syndecan-1, inflammatory factors and PAI-1: Before blood loss, syndecan-1 was significantly higher in the acute high-altitude THS subgroups compared to that in the plain control group ( P<0.05), while no significant differences were observed in IL-6, TNF-α, or PAI-1 ( P>0.05). At 30 minutes after blood loss, syndecan-1, IL-6, TNF-α, and PAI-1 were significantly higher in the acute high-altitude THS subgroups compared to those in the plain control group ( P<0.05). At 120 minutes after blood loss, syndecan-1, IL-6, TNF-α, and PAI-1 were significantly higher in the acute high-altitude THS subgroups compared to those in the plain control group ( P<0.05). Among them, the acute high-altitude THS+0 mg/kg TXA group exhibited significantly higher levels of syndecan-1, IL-6, TNF-α, and PAI-1 compared to the other acute high-altitude THS subgroups ( P<0.05). The acute high-altitude THS+45 mg/kg TXA subgroup had significantly higher syndecan-1, IL-6, and TNF-α compared to those in the acute high-altitude THS+90 mg/kg TXA and acute high-altitude THS+135 mg/kg TXA subgroups ( P<0.05), with no significant difference in PAI-1 ( P>0.05). No significant differences were observed in syndecan-1, IL-6, TNF-α or PAI-1 between the acute high-altitude THS+90 mg/kg TXA and acute high-altitude THS+135 mg/kg TXA subgroups ( P>0.05). (6) Tissue injury: At 6 hours after THS, acute high-altitude THS+0 mg/kg TXA group exhibited significant interstitial thickening of the lung with extensive inflammatory cell infiltration, localized loss of intestinal brush border accompanied by cellular disruption, and marked structural disruption of renal corpuscles with focal cellular injury and necrosis. At 6 hours after THS, the acute high-altitude THS+0 mg/kg TXA subgroup exhibited significantly higher lung injury scores, Chiu′s intestinal injury scores, and kidney injury scores compared to those of the other subgroups ( P<0.05). No significant differences were observed in the tissue injury scores of the lungs, intestines and kidneys among the other subgroups ( P>0.05). The acute high-altitude THS+0 mg/kg TXA subgroup also had significantly higher lung W/D and TLW compared to those in the other subgroups ( P<0.05). At 6 hours after THS, the acute high-altitude THS+45 mg/kg TXA group exhibited significantly higher W/D and TLW of the lung tissues compared to those in the acute high-altitude THS+90 mg/kg TXA and acute high-altitude THS+135 mg/kg TXA groups ( P<0.05), with no significant differences between the latter two subgroups ( P>0.05).

ConclusionsAt 3 days after acute exposure to high altitude, rabbits show a hypercoagulable state of the blood, accompanied by endothelial barrier dysfunction. At 30 minutes after the induction of acute high-altitude THS, a single slow intravenous bolus injection of TXA at doses of 90 mg/kg and 135 mg/kg is more effective in improving coagulation and fibrinolysis function, inflammatory response, endothelial injury, and reduced the risk of pulmonary edema than that at a dose of 45 mg/kg.

High altitude;Shock, traumatic;Hemorrhage;Tranexamic acid
Liu Minghua, Email: nc.defudabe.ummtuil_auhgnim
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引用本文

刘圳,聂超,袁梨嘉,等. 创伤早期不同剂量氨甲环酸治疗急进高原兔创伤失血性休克的效果比较[J]. 中华创伤杂志,2025,41(03)：305-317.

DOI:10.3760/cma.j.cn501098-20240912-00558

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创伤失血性休克（traumatic hemorrhagic shock，THS）是由于躯体遭受严重创伤后，大量失血使有效循环血量急剧减少，进而引起组织灌注不足、细胞缺氧及代谢紊乱的一种临床综合征。THS患者中，25%~35%会发生创伤性凝血病，严重时可因全身凝血因子耗竭发展为弥散性血管内凝血 ［ 1 , 2 ］ ，是临床救治的重点和难点。在急进高原（指人员3 d内从平原快速进入海拔3 000 m以上的高原，或从高原进入更高海拔地区）条件下 ［ 3 ］ ，THS的救治面临更为严峻的挑战。由于高原地区空气稀薄、氧分压低等特点，急进高原后机体的凝血-纤溶系统会发生紊乱，导致血液呈现高凝状态并继发纤溶亢进。随着海拔的上升，凝血-纤溶系统的紊乱程度会更加显著 ［ 4 , 5 ］ ，在THS的基础上，组织器官损伤会因缺氧进一步加重，导致病情进展迅速，且病死率较平原环境显著升高 ［ 6 , 7 ］ 。
氨甲环酸（tranexamic acid，TXA）作为一种抗纤溶药物，可以抑制纤维蛋白分解、稳定现有血凝块，从而达到止血的目的 ［ 8 , 9 ］ 。TXA除抗纤溶外，还具有抑制炎症反应、保护内皮细胞屏障、抑制细胞凋亡和降低血脑屏障通透性等作用 ［ 10 , 11 ］ 。据报道，TXA在颅脑创伤早期使用，可缩短入院后神经重症监护病房（NICU）治疗时间并改善预后 ［ 12 ］ 。目前，临床上推荐在创伤失血3 h内，通过静脉缓慢滴注1 g TXA，随后在8 h内持续滴注1 g TXA，可以减少患者的出血量、输血量并降低病死率 ［ 13 , 14 , 15 ］ 。根据临床指南用药方式，虽能够有效延长药物在血液中的治疗浓度维持时间，但随着研究的深入，研究人员发现单次使用2 g TXA能更有效降低患者的输血需求，患者28 d病死率也更低，而血栓与癫痫事件的发生无明显增加 ［ 8 ， 16 , 17 , 18 ］ 。此外，美军战场战术救护（TCCC）指南根据美军实际使用情况反馈，已将TXA单次使用剂量提高为2 g ［ 19 ］ 。目前，尚无研究系统评价急进高原发生THS后，使用不同剂量TXA的临床疗效差异，故急进高原THS患者的有效救治存在不确定性。鉴于此，笔者采用兔急进高原THS模型，比较不同剂量TXA治疗急进高原THS早期的疗效差异，为急进高原THS患者TXA的使用剂量提供实验依据。
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备注信息
A
刘明华，Email： nc.defudabe.ummtuil_auhgnim
B

刘圳：研究实施、数据整理及统计学分析、论文撰写及修改；聂超、袁梨嘉：研究实施、数据收集；杨玲、蒋慧、钱程、蔡凌虎、张翼：技术指导及结果分析；刘明华：研究指导、论文修改、经费支持

C
刘圳, 聂超, 袁梨嘉, 等. 创伤早期不同剂量氨甲环酸治疗急进高原兔创伤失血性休克的效果比较[J]. 中华创伤杂志, 2025, 41(3): 305-317. DOI: 10.3760/cma.j.cn501098-20240912-00558.
D
所有作者声明不存在利益冲突
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