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hemorrhagic shock model
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  失血性休克模型
     Hemorrhagic shock model was established in rabbits in groups L and H, and the venous blood samples were collected for measurement of plasma malondialdehyde (MDA) and superoxidedismutase (SOD) before phlebotomy (T0), 2 h after hemorrhagic shock (T1) and 2 h after resuscitation (T2).
     L组于放血前静脉注射2.5mg/kg利多卡因,此后每隔1h静脉注射1mg/kg利多卡因维持; L组与H组建立失血性休克模型后,分别于放血前(T0)、休克2h(T1)、复苏2h(T2)各从股静脉取血测定血浆丙二醛(MDA)、超氧化物歧化酶(SOD);
短句来源
     Methods: 1. Hemorrhagic shock model: Wister rats(250-300g) were anesthetized with 4.5% amobarbital sodium(80mg/Kg i.p.) in room temperature(25℃).
     实验方法:1.失血性休克模型的建立:Wister大鼠(体重250-300g)雌雄不限,用4.5%异戊巴比妥(80mg/kg)在25℃室温下腹腔内给药麻醉。
短句来源
     Methods Fifty healthy male SD rats were randomly divided into the sham group(SHA group,n=10),the Ringer′s solution group(RS group,n=20) and 6% hydroxyethyl saline group(HES group,n=20). (Controlled) hemorrhagic shock model was reproduced in RS and HES groups.
     方法50只健康雄性SD大鼠按随机数字表法分为假手术组(SHA组,n=10)、RS组(n=20)、HES组(n=20),RS组和HES组制备可控性失血性休克模型
短句来源
     Methods After the canine-modified Wiggers'hemorrhagic shock model was successfully duplicated,the animals were randomized to two groups,receiving 7. 5% Saline plus Dex (HSD)6 ml/kg. BW in 5 minutes at 10 minutes (Group 1) and 70 minutes (Group 2).
     方法 采用修订的Wiggers法复制犬失血性休克模型后,将实验动物随机分为两组,分别于休克后 10 min(组1)、70 min(组2)给予 6ml/kg 7.5%NaCl右旋糖酐溶液(HSD)静推,5min内输完。
短句来源
     Methods The rats were divided into 3 groups: a normal group (n=10), a control group (n=40) and a preconditioning group (n=40). Pinacidil preconditioning was processed 24 h before making the hemorrhagic shock model.
     方法  (1)大鼠 90只 ,随机分为正常组 (N组 ,10只 )、对照组 (C组 ,40只 )和预处理组(PC组 ,40只 ) ,PC组大鼠用Pinacidil进行预处理 ,2 4h后将对照组和预处理组大鼠复制成失血性休克模型 ,用Westernblot方法观察不同时相点大鼠心肌组织细胞型磷脂酶A2 (cPLA2 )的表达变化 ;
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  “hemorrhagic shock model”译为未确定词的双语例句
     The traumatic hemorrhagic shock model was reproduced by producing femur fracture and femoral artery bleeding to reduce the mean artery pressure to (40±5) mm Hg(1 mm Hg= 0.133 kPa).
     动物模型用经股动脉放血使平均动脉压降至 (40±5)mm Hg(1 mm Hg=0.133 kPa).
短句来源
     Methods After the rabbit hemorrhagic shock model was successfully duplicated, the 30 rabbits were randomized to four groups, receiving hypothermic fluid (10.7±1.6℃), normothermic fluid (20.6±1.3℃), hyperthermic fluid (39.5±1.3℃) and autoblood.
     方法选择健康新西兰雄兔30只,随机分为4组进行手术插管及制作休克模型,在休克模型稳定30min后按相同速度相同液量分别给予低温(10.7±1.6)℃、常温(20.6±1.3)℃及温热(39.5±1.3)℃平衡液和自体血;
短句来源
     Methods:After the rabbit hemorrhagic shock model was successfully duplicated, the 30 rabbits were randomized to four groups, receiving hypothermic fluid(10.7±1.6)℃, normothermic fluid(20.6±1.3)℃and hyperthermic fluid(39.5±1.3)℃.
     方法 :选择健康新西兰雄兔 30只 ,随机分为 4组进行手术插管及制作休克模型 ,在休克模型稳定30min后按相同速度相同液量分别给予低温 (10 .7± 1.6 )℃、常温 (2 0 .6± 1.3)℃及温热 (39.5± 1.3)℃平衡液和自体血 ;
短句来源
     Methods After the rabbit hemorrhagic shock model was successfully duplicated,the 30 rabbits were randomized to four groups,receiving hypothermic fluid(10.7±1 6℃),normothermic fluid(10.7±1 3℃) and hyperthermic fluid(39.5±1 3℃).
     方法健康新西兰雄兔 30只 ,随机分为 4组进行手术插管及制作休克模型 ,在休克模型稳定 30min后按相同速度、相同液量分别给予低温 (1 0 .7± 1 .6℃ )、常温 (2 0 .6± 1 .3℃ )及温热(39.5± 1 .3℃ )平衡液和自体血 ;
短句来源
     Method: After the rabbit hemorrhagic shock model was successfully duplicated, the 30 rabbits were randomized to four groups, receiving hypothermic fluid(10.7±1.6 ℃), normothermic fluid(20.6±1.3 ℃)and hyperthermic fluid(39.5±1.3℃).
     方法 :新西兰雄兔 3 0只 ,随机分为 4组制作休克模型 ,休克模型稳定 3 0min后按相同速度相同液量分别给予低温 ( 10 .7± 1.6℃ )、常温 ( 2 0 .6± 1.3℃ )及温热 ( 3 9.5± 1.3℃ )平衡液和自体血 ;
短句来源
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  相似匹配句对
     shock;
     ②休克;
短句来源
     Shock
     休克
短句来源
     The Treatment of Hemorrhagic Shock with Mannitol
     高渗甘露醇抢救失血性休克42例分析
短句来源
     The effect of aminoguanidine in prolonged hemorrhagic shock
     氨基胍在兔重度失血性休克中的治疗价值
短句来源
     The model of hemorrhagic shock resuscitation was used.
     采用失血性休克复苏动物模型。
短句来源
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  hemorrhagic shock model
The conscious, unrestrained and cumulative volume-controlled hemorrhagic shock model was a good experimental model to investigate the physical phenomenon without anesthetic interfernce.
      
Using a rat systemic hemorrhagic shock model, injury to the central organs, being the brain, heart, lungs, liver, and kidneys was assessed by measuring malondialdehyde (MDA).
      
All 3 regimens were equally efficacious in providing initial metabolic recovery in this experimental hemorrhagic shock model.
      
HES storage in healthy animals was not associated with signs of either inflammation or apoptosis contrary to a previously described animal hemorrhagic shock model.
      
Using uptake volumes of various degrees in a hemorrhagic shock model as the endpoint of the hypotensive stress, it seems possible to produce reliable survival rates.
      
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An irreversible hemorrhagic shock model was reproduced in rats. The change of microcirculation of cremaster muscle was observed by a Hitachi colour microscopic TV set.In saline-treated group(N=12) , 1h after hypotension(BP 40 mmHg) , 0.5 ml of normal saline was given i.v., followed by reinfusion of the shed blood. In polygonum cuspidatum-treated group, crystal No 4 of polygonum cus-pidatum ( P.C. ) was given in three different dosages, viz. 0.5, 1.0 and 2.0mg/ 100g b.w. ( N=8 for each dosage) . Administration...

An irreversible hemorrhagic shock model was reproduced in rats. The change of microcirculation of cremaster muscle was observed by a Hitachi colour microscopic TV set.In saline-treated group(N=12) , 1h after hypotension(BP 40 mmHg) , 0.5 ml of normal saline was given i.v., followed by reinfusion of the shed blood. In polygonum cuspidatum-treated group, crystal No 4 of polygonum cus-pidatum ( P.C. ) was given in three different dosages, viz. 0.5, 1.0 and 2.0mg/ 100g b.w. ( N=8 for each dosage) . Administration of P.C. and transfusion of the shed blood made the narrowed arterioles restore to nearly normal, blood capillaries reflow, and blood pressure remain stable. For example , the diameter of A2 in cremaster muscle changed from G4.5 ±4.9% of the normal value at 1h after hypotension to 91.7±4.2% at 2h after treatment, As from 59.6±4.6% to 100.7± 6.6% in the P.C. treated group. However, in saline-treated group, blood pressure trended to fall dowm gradually and no complete restoration of microcircula-tion was observed 2h after treatment.The diameter of A2 changed from 64.1±3.6% to 65.9 ± 5.2%,that of A2rom 66.3±3.7% to 72.3±5.2% at 2h after saline infusion. Topical application of P.C. also made arterioles dilate. The 24h survival rate in P.C. treated group(23/24)was significantly higher than that in saline-treated group ( 2/12) . It is shown in our study that P.C. is a very effective drug to ameliorate the microcirculatory disorders and to increase survival rate in shock animals.

本文观察了虎仗4号结晶对大鼠不可逆性失血性休克时血压的影响,用彩色显微电视装置观察了提睾肌微循环的变化.结果表明,静脉注入不同剂量的虎仗4号结晶和回输放出的血液后,可使动物血压稳定上升,使休克时缩窄的细动脉口径恢复,毛细血管开放,动物存活率明显提高;虎仗4号结晶的作用效果与剂量增加有一致的趋势.讨论了虎仗4号结晶的作用机理.

This paper reports the effect of captopril (SQ14225)on hemorrhagicshock in rabbits.After a hemorrhagic shock model was replicated,the rabbits wererandomly divided into a captopriltreated group (n=13) and a control group(n=13).In the treated group,intravenous drip of captopril (lmg/1kg) was performed withnormal saline (15ml/kg),low molecular dextran (15ml/kg) and blood.An hour later,MABP,CVP and renal blood flow were elevated to nearly normal level and mesentl-eric microcirculation was obviously improved,the...

This paper reports the effect of captopril (SQ14225)on hemorrhagicshock in rabbits.After a hemorrhagic shock model was replicated,the rabbits wererandomly divided into a captopriltreated group (n=13) and a control group(n=13).In the treated group,intravenous drip of captopril (lmg/1kg) was performed withnormal saline (15ml/kg),low molecular dextran (15ml/kg) and blood.An hour later,MABP,CVP and renal blood flow were elevated to nearly normal level and mesentl-eric microcirculation was obviously improved,the difference between the controand the treated group was very significant (p<0.01).The results show that captop-ril is effective against hemorrhagic shock.

本文报告了巯甲丙脯酸对家兔失血性休克的作用。复制家兔失血性休克模型后,将动物随机分为巯甲丙脯酸治疗组和对照组。结果表明:在治疗组,静滴巯甲丙脯酸1mg/kg 及配合输液输血后,平均动脉血压、中心静脉压、肾血流量均见明显回升,肠系膜微循环有显著性改善,1小时接近正常水平;与对照组相比差异有高度显著性意义(p<0.01)。认为巯甲丙脯酸具有良好的抗失血性休克作用。

A dog hemorrhagic shock model was created by blood-lost through the femoral artery and dog histaminia model reproduced by intravenous admlnistration of histamine. Plasma levels of TXB2 and 6-Keto-PGF_1α increased in both.A negative correlation was showed between the changes of the plasma concentration of TXB2 and 6-Keto-PGF_1α and the change of the blood pressure. The injection of adrenaline increased both the blood pressure and the plasma TXB2 and 6-Keto-PGF_1α in the shock models. This...

A dog hemorrhagic shock model was created by blood-lost through the femoral artery and dog histaminia model reproduced by intravenous admlnistration of histamine. Plasma levels of TXB2 and 6-Keto-PGF_1α increased in both.A negative correlation was showed between the changes of the plasma concentration of TXB2 and 6-Keto-PGF_1α and the change of the blood pressure. The injection of adrenaline increased both the blood pressure and the plasma TXB2 and 6-Keto-PGF_1α in the shock models. This observation led us to speculate that the increased plasma TXB2 might cause a vicious disturbance of microcirculation and the increased plasma 6-Keto-PGF_1α might mediate an arterial hypotension in both.

本文观察了出血性休克和应用回输血治疗及组胺性休克应用肾上腺素治疗时,犬血浆血栓素B_2(TXB_2)和6-酮-前列腺素F_1α(6-Keto-PGF_1α)的变化。在这两种休克模型中,血浆中FXB_2和6-Keto-PGF_1α均明显升高.血浆中TXB_2升高可能成为导致微循环恶化的重要因素,6-Keto-PGF_1α升高可介导血压下降.这两种物质增多均可能促进休克的持续发展.

 
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