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injury     
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  损伤
    Studies on the Mechanism of Imbalance of Inflammatory Mediators and Anti-inflammatory Mediators in the Development of Acute Lung Injury by Endotoxin and the Protective Effects of Interleukin-10 and Dexamethasone
    内毒素致急性肺损伤中炎症介质/抗炎介质失衡机制及白介素10、地塞米送的保护作用
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    Investigation of Mechanism of Cell Signal Transduction and Protective Role of Dexamethasone in Acute Lung Injury Rat
    急性肺损伤大鼠细胞信号转导机制及地塞米松保护作用的研究
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    Effect of RNA Interference on TLR4 Signaling Pathway in Alveolar Macrophage of Acute Lung Injury Rat Induced by Lipopolysaccharide
    RNAi对内毒素急性肺损伤大鼠肺泡巨噬细胞TLR4信号通路的影响
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    A Study of Cell Membrane Damage after Severe Traumatic Brain Injury and the Effect of Hypothermia on It
    重型脑创伤后细胞膜损伤及亚低温对其影响的研究
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    Experimental Studies for the Prevention Effects of Intraperitoneal or Intravenous Injection with Perfluorocarbon in Rat with Acute Lung Injury
    腹腔或静脉注射全氟化碳对大鼠急性肺损伤预防作用的实验研究
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    Mechanism and Role of Aquaporin 4 in Brain Edema Formation Resulting from Brain Explosive Injury
    AQP4在颅脑爆炸后脑水肿发生机制中的作用研究
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    The Roles and Mechanism of Adenosine A2A Receptors in Acute Stage of Traumatic Brain Injury
    腺苷A2A受体在脑撞击急性期的作用及机制研究
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    The Experimental Study on the Construction of Skin Sheet with Two Kinds of Gene Modified Cells and Its Employment in Promoting the Healing of Wound-Radiation Combined Injury
    两种细胞基因修饰皮片构建与促进放创复合创面愈合的实验研究
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    Study on Treatment of Severe Brain Injury with Nanoparticles as Gene Carriers of TNF-alpha Antisense Oligonucleotide
    TNF-alpha反义寡核苷酸纳米粒子治疗重型颅脑的实验研究
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    Results①PaO_2 increased significantly since 1 hour after inhalation injury,and rabbits had better arterial oxygenation within 4 hours. PaO_2 and PO_2 a/A in HFOV group were better than those in CMV group since 2 hours after inhalation injury,and there existed significant difference.
    结果①HFOV组和CMV组PaO_2均在后1 h明显上升,后4 h内动脉血仍有良好氧合,自后2 h点动脉血氧合和PO_2a/A,HFOV组明显优于CMV组,差异具有统计学意义(P<0.01);
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  外伤
    Experimental Research of Expression and Significance of P-selectin, ICAM-1 and Influence of EGB after Brain Injury in Rats
    大鼠脑外伤后脑组织P-selectin、ICAM-1表达及EGB干预作用的实验研究
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    The effective rate (91.35%) of HBO on the patients who began to receive HBO when they had subjected injury for less 1 month was the highest than the other groups (P<0.05).
    首次HBO治疗距离外伤时间<1个月的患者有效率为91.35%,与其他组比较最高(P<0.05)。
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    Objective ①To investigate the variable levels of serum S-100B protein in patients with brain injury.
    目的①探讨颅脑外伤后血浆S-100B蛋白变化规律;
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    Conclusion Electrocardiogram was considered to be reference indexes in judging the condition and prognosis of patients with acute cerebral injury, abnormal electrocardiogram indicated bad prognosis.
    结论急性脑损伤患者急性期极易产生脑心综合征。 ECG变化异常可作为判断急性脑外伤早期预后的一项参考指标。
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    objectiveTo elucidate the diagnosis and treatment of cardiac injury elicited by traumatic chest injury.
    目的总结胸部外伤致心脏损伤的诊断与治疗经验。
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  创伤
    Establishment of Severe Traumatic Brain Injury Model Induced by Fluid Percussion in Rabbits and the Effects of Posttraumatic Mild Hypothermia Therapy
    兔液压冲击重型脑创伤模型的建立及亚低温治疗的影响
短句来源
    A Study of Cell Membrane Damage after Severe Traumatic Brain Injury and the Effect of Hypothermia on It
    重型脑创伤后细胞膜损伤及亚低温对其影响的研究
短句来源
    Role of GR and NF-κB in the Hepatic Injury and Its Mechanisms in Rats Subjected to Severely Traumatic Shock
    GR及NF-κB在严重创伤休克大鼠肝损伤中的作用及其机理
短句来源
    Role of Immune Response in the Secondary Injury after Brain Trauma in Rats
    免疫应答在大鼠脑组织创伤后继发性损伤中的作用
短句来源
    A Study of Atrial Natriuretic Peptide, Angiotensin Ⅱ Changes and Mechanism to Traumatic Brain Edema during Acute Head Injury
    急性颅脑损伤ANP,AngⅡ变化及对创伤性脑水肿的作用机理研究
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  injury
Our studies demonstrated an in vivo cardioprotection effect of (N-(3,4,-dimethoxy-2-chlorobenzylideneamino)-guanidine: ME10092) in ischaemic reperfusion injury in the rodent.
      
Diclofenac (25 mg kg-1) and meloxicam (7.5 mg kg-1) produced 9.3 and 19.6 mm2 ulcer areas in stomachs of rats, respectively, when used alone, but when combined with nimesulide diclofenac and meloxicam did not cause any injury in rat stomachs.
      
These proteins may be involved in cardiovascular injury, and could play an important role in the treatment of coronary heart disease.
      
SOD and POD activities declined correspondingly, followed by significant increases of MDA and MP, and leaf injury was finally observed.
      
Hepatocellular injury was the predominant type in these cases (132 cases, 48%).
      
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Objective: In order to investigate the significance of mechanism of the reperfusion injury in hemor-rhagic shoc.Methods: The changes of MDA and superoxide dismutase (SOD)in various tissues and activityof lysosomal hydrolases in plasma of rat in sustained hemorrhagic shock for 3 h and reperfused for 1.5 h afterhemorrhage 1.5 h were measured and compared, the effect of pretreatment with exogenous SOD and catalase(Cat) was also evaluated. Results: In reperfused rats, the cellular damage was much more severe...

Objective: In order to investigate the significance of mechanism of the reperfusion injury in hemor-rhagic shoc.Methods: The changes of MDA and superoxide dismutase (SOD)in various tissues and activityof lysosomal hydrolases in plasma of rat in sustained hemorrhagic shock for 3 h and reperfused for 1.5 h afterhemorrhage 1.5 h were measured and compared, the effect of pretreatment with exogenous SOD and catalase(Cat) was also evaluated. Results: In reperfused rats, the cellular damage was much more severe than thatoccured in sustained hemorrhage rats,the levels of MDA and lysosomal hydrolases increased significantly(P<0. 01) and levels of SOD obviously decreased (P<0.01). Pretreatment with combination of SOD and Catwas very effective in attenuating the reperfused injury.Conclusion : The mechanism of ischemia and reperfu-sion injury resulting from oxygen free radicals may be a primary factor of irreversible shock, which has an im-portant clinical significance for the shock rescue.

目的:为探讨再灌注损伤机制在失血性休克中的意义.方法:作者采用失血性休克大鼠实验模型,测定和比较了大鼠不同脏器中丙二醛(MDA),超氧化物歧化酶(SOD)含量和血浆溶酶体水解酶活性在失血休克3h,失血1.5h后再灌注1.5h的改变以及外源性SOD和过氧化氢酶(Cat)的防治再灌注损伤的效果.结果:失血性休克后快速再灌注,各脏器组织中MDA和血浆溶酶体酶明显增高(P<0.01),SOD显著下降(P<0.01),细胞损伤明显重于对照组动物;联合应用SOD和Cat预防治疗,有效地减轻了再灌注后组织损伤.结论:氧自由基在缺血再灌注中的这种细胞损伤机制,可能是不可逆性休克的一个主要原因,具有重要的临床指导意义.

A model of hemorrhagic shock was reproduced in dogs. The level of plasma MDA and the activity of blood SOD were measured. The effect of external counterpulsation (EC) on the activity of blood SOD and the level of plasma MDA in hemorrhagic shock were observed. The results showed that the content of plasma MDA was increased and the activity of blood SOD was decreased apparently after hemorrhagic shock, and the increasing MDA level was returned to normal and the activity of decreased SOD was improved by administration...

A model of hemorrhagic shock was reproduced in dogs. The level of plasma MDA and the activity of blood SOD were measured. The effect of external counterpulsation (EC) on the activity of blood SOD and the level of plasma MDA in hemorrhagic shock were observed. The results showed that the content of plasma MDA was increased and the activity of blood SOD was decreased apparently after hemorrhagic shock, and the increasing MDA level was returned to normal and the activity of decreased SOD was improved by administration of EC. The conclution is that EC treatment does not cause reperfusion injury, and may decrease the production of free radicals during hemorrhagic shock.

作者复制犬失血性休克模型。用改良的硫代巴比妥酸法测定血浆丙二醛(MDA)含量,用光化学扩增法测定全血超氧歧化酶(SOD)活性。观察WFB—Ⅴ型电脑控制的增强型体外反搏机治疗失血性休克后对上述指标的影响。结果表明,犬失血性休克后血浆MDA明显升高,全血SOD活性显著下降。体外反搏治疗可使升高的MDA含量降至正常水平,SOD活性明显恢复,从而证明体外反搏治疗失血性休克时,并没有因微循环灌流的改善而带来再灌流损伤,反而能使休克时氧自由基产生减少,为临床应用体外反搏治疗休克提供了理论基础。

Twelve mongrel dogs, anesthetized with pento-barbital, were bled to a main atrial pressure (MAP) of 40 mmHg within 30 minutes and kept at this level for 30 minutes, then the changes of serum angiotensin Ⅱ (AGTⅡ ) /atrial natriuretic peptide (ANP) were observed before and after treatment with 7.5% NaCl/ 4. 2% dextran 40 (HSD) and lactate sodium ringer (LR). The results showed that AGT Ⅱ /ANP increased significantly during shock (from 72. 71 ± 18. 54 to 479. 31 ± 126. 25 n= 6 P<0. 001), and AGTⅡ /ANP was out...

Twelve mongrel dogs, anesthetized with pento-barbital, were bled to a main atrial pressure (MAP) of 40 mmHg within 30 minutes and kept at this level for 30 minutes, then the changes of serum angiotensin Ⅱ (AGTⅡ ) /atrial natriuretic peptide (ANP) were observed before and after treatment with 7.5% NaCl/ 4. 2% dextran 40 (HSD) and lactate sodium ringer (LR). The results showed that AGT Ⅱ /ANP increased significantly during shock (from 72. 71 ± 18. 54 to 479. 31 ± 126. 25 n= 6 P<0. 001), and AGTⅡ /ANP was out of balance. At the begining of resuscitation, HSD elevated MAP rapidly,and produced a rapid dramatic reduction in AGTⅡ (479. 31 = 126. 25 vs 66. 13±22. 13 n=6 P<0.001), and AGT Ⅱ / ANP also deccreased significantly at one hour after resuscitation compared with LR (P < 0. 05). The experiment showed that HSD can relieve microvascular spasm in time, improve microcirculation, shorten ischemia/reperfusion injury. The main mechaism is probably that HSD can rapidly recover the balance of endogenous injury and antiinjury factor, moreover, it is an essential element that high concentration of Na+ stimulates the macula densa, inhibiting renin secrete.

本研究采用特异性的放免法测定 7. 5%氯化钠/4. 2%右旋糖酐 40(HSD)和 0. 9%乳酸钠林格氏液(LR)治疗犬严重失血性休克前后血浆中血管紧张素 Ⅱ(AGTⅡ)和心钠素(ANP)含量的变化,发现HSD较LR能在快速提高平均动脉压(MAP)的同时迅速恢复AGTⅡ/ANP的平衡,及早地解除微血管痉挛,缩短缺血时间,减轻缺血再灌注损伤。本实验提示:HSD快速恢复内源性损伤和抗损伤物质的平衡,可能是其抗休克的主要机制,而且高浓度Na+刺激肾小管致密斑,抑制肾素分泌可能是HSD抗休克的基本因素。

 
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