创伤性休克

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  • traumatic shock
创伤性休克创伤性休克
  1. NOS抑制剂对创伤性休克作用的实验研究

    The experimental research of NOS inhibitor effect on the survival rates of rats with traumatic shock

  2. 创伤性休克与全身性炎症反应IL-10的升高可能系炎症早期的一种代偿性反应。

    Traumatic shock and systemic inflammation Elevation of IL 10 may be a compensational reaction of early inflammation .

  3. 死亡原因均为合并伤伴创伤性休克或感染性休克,导致MODS。

    The death causes was MODS resulted from traumatic and infections shock .

  4. 伤后24h内死于失血性、创伤性休克、多脏器功能衰竭8例;

    Cases died of hemorrhagic shock , wound shock , MODS in 24 hours after trauma ;

  5. 方法检测38例不同类型的SIRS(创伤、创伤性休克、感染性休克)患者及12例健康对照组血浆TNF-a、NE、ET、ADM水平。

    Methods Plasma TNF-a , NE , ET and ADM levels were measured in 38 patients with SIRS .

  6. 创伤性休克病人单个核细胞表面Mac&1、CD18的表达

    Surface Expression of Mac 1 , CD 18 on Mononuclear Cell in Traumatic Shock

  7. 目的观察创伤性休克兔血浆一氧化氮(NitricOXide,NO)的动态变化及鸟苷酸环化酶抑制药亚甲蓝(methyleneblue,MB)的干预作用。

    Objective To observe the changes of plasma nitric oxide in rabbits with traumatic shock and the intervention of methylene blue ( MB ), a guanylate cyclase inhibitor .

  8. 小鼠创伤性休克时血中糖、乳酸和NPN变化的发生

    Alterations of plasma glucose , lactate and NPN in mouse traumatic shock

  9. 目的探讨创伤性休克患者血浆P选择素(PSel)、血管内皮生长因子(VEGF)和一氧化氮(NO)的含量变化及其意义。

    Objective To detect the role of P-Selectin ( P-Sel ), vascular endothelial growth factor ( VEGF ) and nitric oxide ( NO ) on the etiology of traumatic shock .

  10. 故用于创伤性休克的治疗,TRH比纳洛酮更合适。

    So TRH would be a better choice than naloxone in the treatment of traumatic shock .

  11. 人创伤性休克时白细胞表面LFA-1、Mac-1、CD18的表达

    Surface Expression of LFA-1 , Mao-1 and CD18 on Leukocyte in Human Traumatic Shock

  12. 创伤性休克大鼠中性粒细胞CD18、糖皮质激素受体的变化及纳洛酮治疗作用的研究

    Studies on expression of neutrophil CD18 、 glucocorticoid receptor and therapeutic effects of naloxone in traumatic shock of rats

  13. 方法动态监测47例创伤性休克患者血LBP浓度,并对发生全身炎症反应综合征(SIRS)或MODS的患者连续抽血3次培养进行细菌学检查。

    Methods : LBP in 47 traumatic shock patients was monitored dynamically . The patients with SIRS or MODS were taken blood bacteriology detection 3 times .

  14. 结论:早期低压液体复苏可降低创伤性休克患者的死亡率,其中休克后1~2h内控制输液量是救治的关键。

    Conclusion : Hypotensive fluid resuscitation can reduce the mortality of traumatic hemorrhagic shock , and controlling transfusion volume from 1h to 2h was the key for cure .

  15. 目的探讨创伤性休克家兔血浆血栓素A2(TXA2)和前列环素(PGI2)的变化以及葛根素的调控作用。

    Objective To investigate the changes of Plasma TXA2 and PGI2 Levels of Rabbits with Traumatic Shock and the effects of puerarin on them .

  16. 用单克隆抗体间接免疫荧光标记法测定创伤性休克病人单个核细胞表面Mac-1、CD18的表达。

    Using indirect immunofluorescence method , the surface expression of Mac 1 and CD 18 on human mononuclear cell were investigated in traumatic shock .

  17. 探讨纳洛酮(NAL)在创伤性休克治疗中的作用与机制。

    The purpose of this study was to evaluate the effect and mechanism of naloxone ( NAL ) in the treatment of traumatic shock .

  18. 目的调查分析创伤性休克患者院前救治与术后急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)的相关性及其临床意义。

    Objective To investigate and analyze the correlation and clinical significance of prehospital treatment for traumatic shock and postoperative acute lung injury ( ALI ) / acute respiratory distress syndrome ( ARDS ) .

  19. 方法检测250例创伤性休克的患者(其中72例并发DIC)的PT、APTT、D-D、FDP、3P试验,并分析比较这些试验结果的表达水平及探讨创伤性休克患者并发DIC的相关性。

    Methods AP , APTT , D-D , FDP and3P test were performed in250 cases of traumatic shock ( 72 cases complicated with DIC ) . The correlation between the test results and DIC was analyzed .

  20. 方法:40只Wistar大鼠制作创伤性休克动物模型,双侧股骨干砸伤后并经股动脉放血至平均动脉压(MAP)35~45mmHg(467~600kPa),维持30min,然后回输失血和等量的林格式液。

    Methods : Animal models of traumatic shock were established in 40 Wistar rats following fractures in both femur shafts and subsequent depletion until the mean arterial pressure in the femoral artery dropped to 35 to 45mmHg ( 4.67 ~ 6.00kPa ) .

  21. 目的探讨创伤性休克兔中性粒细胞黏附分子CD11b、血清可溶性细胞间黏附分子(sICAM)1的动态变化及不同复苏液的影响。

    Objective To investigate the changes of polymorphonuclear neutrophil adhesive molecule CD11b and serum soluble intercellular adhesion molecule 1 ( sICAM 1 ) and influences of various resuscitation fluids in traumatic shock in rabbits .

  22. 结果:正常大鼠肺泡巨噬细胞表达一定水平的IL-18mRNA,而遭受创伤性休克打击后,肺泡巨噬细胞IL-18mRNA表达迅速升高,4h达高峰,8h后即恢复到正常水平。

    Result : AM of normal rats expressed IL 18 mRNA to some extent ; expression of IL 18 mRNA increased quickly with peak levels being present 4h after trauma combined with hemorrhagic shock , and returned to baseline levels 8h later .

  23. 检测休克前、休克后0.5h、1.5h、3h和4h5个时间点血清cTnI的水平,观察创伤性休克家兔在休克过程中cTnI的动态变化。

    The levels of serum cTnI were measured at pre-shock , 0.5 hours , 1.5 hours , 3 hours , and 4 hours after shock . The dynamic changes of cTnI were scrutinized in rabbits with traumatic shock during the shock process .

  24. 74只成年健康雄性家兔,用改良的钳压法和wiggers法造成深度创伤性休克动物模型。

    Deep shock animal models were produced in 74 adult rabbits using the method of pincers pressure and Wiggers ' hemorrhagic shock method to produce crush injury of the soft tissue on the thigh and comminuted fracture of the femur .

  25. 创伤性休克大鼠血浆P-选择素的变化及意义

    Alternation and Significance of P-selectin in Plasma During Rats Traumatic Shock

  26. 创伤性休克患者黏附分子的变化及意义

    Alteration and significance of adhesion molecule in traumatic shock patients

  27. 创伤性休克术前限制性液体复苏对患者的影响

    Influence of preoperative limited fluid resuscitation on traumatic shock patients

  28. 目的制作兔创伤性休克模型。

    Objective To establish the traumatic shock model in rabbit .

  29. 方法采用Lamson's法建立家兔创伤性休克模型。

    Methods The traumatic shock model wa established applying Lamson 's method .

  30. 创伤性休克早期低压液体复苏的临床探讨

    Clinical Analysis of Hypotensive Fluid Resuscitation on Traumatic Hemorrhagic Shock