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acute ischemic injury
相关语句
  急性脑缺血
     Protective Effect of Electroacupuncture Against Acute Ischemic Injury and the Possible Involvement of Taurine
     针刺督脉穴位抗急性脑缺血的效应及其与牛磺酸的关系
短句来源
  急性缺血再灌注损伤
     Effect of Ischemic Postconditioning and Pharmacological-conditioning Induced by ATP after Acute Ischemic Injury
     缺血后处理和ATP药物后处理对兔急性缺血再灌注损伤心肌的保护作用
短句来源
  “acute ischemic injury”译为未确定词的双语例句
     Renal Ischemic Preconditioning Attenuate Acute Ischemic Injury in Rat Kidney and Its Mechanism
     大鼠肾脏缺血预适应现象的证实及其机制研究
短句来源
     Changes of cholinergic nerve morphosis and density in the left ventricle of rats after acute ischemic injury induced by myocardial infarction
     大鼠心肌缺血性损伤后胆碱能神经形态及密度观察
短句来源
     Objective To study the effects of intracerebrovertricular injection of nalorphine on the Ca 2+ ATPase activity in cerebral ischemia rats and discuss the protective mechanism of nalorphine on acute ischemic injury rats.
     目的 观察脑室注射纳洛酚对脑缺血大鼠大脑皮层体感区Ca2 + ATP酶活性的影响 ,探讨纳洛酚对急性大鼠脑缺血性损伤的保护机制。
短句来源
     EFFECT OF ISCHEMIC POSTCONDITIONING ON MYOCARDIAL BIOCHEMICAL INDEXES AFTER ACUTE ISCHEMIC INJURY
     缺血后处理对急性缺血再灌注心肌生化指标的影响
短句来源
     ST segment elevation in epicar-dial electrogram was used as a criterion of acute ischemic injury.
     2)心外膜ST段抬高作为急性心肌缺血的指标;
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  相似匹配句对
     Pathogenesis of acute focal ischemic cerebral injury
     急性局灶性脑缺血性脑损伤发生机制
短句来源
     acute lung injury;
     急性肺损伤;
短句来源
     The Ischemic Injury of Oligodendrocytes
     少突胶质细胞缺血性损伤
短句来源
     The Mechanism of Microirculatory Disturbance in Acute Cerebral Ischemic Injury
     急性脑缺血损伤的微循环障碍机制
短句来源
     Mechanism of Bajisin's Protective Effect on Acute Cerebral Ischemic Injury
     巴戟素对急性缺血性脑损伤保护作用的机制研究
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  acute ischemic injury
PURPOSE: We report two cases of spontaneous anal passage of a large bowel 'cast' caused by acute ischemic injury.
      
We present evidence suggesting that gap-junctional hemichannels (GJH) may be involved in acute ischemic injury of human renal proximal tubule cells (hPT cells).
      
These are regeneration following acute ischemic injury and the process of cystogenesis in polycystic kidney disease.
      
Animal and human studies have been used to monitor the different steps in the development of acute ischemic injury on a cellular level.
      
In pioneering studies, Pepys and colleagues demonstrated that human CRP promotes myocardial infarction in a rat model of acute ischemic injury.
      
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To assess the role of adenosine receptors in the cardioprotective effect of preconditioning and the characterization of adenosine receptors in heart. METHODS: In 18 anesthetized rabbits, myocardial ischemia was induced by occlusion of left descending coronary artery. ST segment elevation in epicar-dial electrogram was used as a criterion of acute ischemic injury. Myocardial adenosine receptors were measured using [3H]adenosine ligand. RESULTS:After 60-min ischemia, epicardial ST segment elevation was higher...

To assess the role of adenosine receptors in the cardioprotective effect of preconditioning and the characterization of adenosine receptors in heart. METHODS: In 18 anesthetized rabbits, myocardial ischemia was induced by occlusion of left descending coronary artery. ST segment elevation in epicar-dial electrogram was used as a criterion of acute ischemic injury. Myocardial adenosine receptors were measured using [3H]adenosine ligand. RESULTS:After 60-min ischemia, epicardial ST segment elevation was higher in ischemia group (13.9±0.6mV) than in the ischemic preconditioning group (3.1 ±0.5mV). In membranes of the ventricular myocytes prepared from ischemic-precondi-tioning group, the density of adenosine receptors was higher than that of ischemia and sham ischemia groups (Bmax being 602±40, 348±28, and 335±30pmol/g protein, respectively). Affinity of the receptors for the [3H] adenosine was not different in the 3 groups (Kd being 181±18, 169±21, and 196 ±24nmol.L-1,respectively). CONCLUSION:Activation of adenosine receptors along with an increase in adenosine receptor density during ischemic-preconditioning provides the basis for adenosine to exert its protective effect on the ischemic heart.

分析腺苷受体在预缺血对心肌保护中的作用和心肌腺苷受体的特性.方法:1)在18只麻醉家兔,结扎左冠脉前降支以诱发心肌缺血;2)心外膜ST段抬高作为急性心肌缺血的指标;3)用[~3H]腺苷测定心肌腺苷受体.结果:1)缺血60 min时,心外膜ST段抬高(13.9±0.6 mV)明显高于预缺血后再缺血60 min时(3.1±0.5 mV);2)在预缺血后再缺血心室肌细胞膜,腺苷受体密度(B_(max))高于单独缺血组和对照组(B_(max)分别为602±40,348±28和335±30 pmol/g protein),但缺血组的心室肌细胞膜腺苷B_(max)未增高;3)各组的心室肌细胞膜的腺苷受体亲合力(K_d无显著差异(K_d分别为181±18,169士21和196±24 nmol·L~(-1)).结论:预缺血时腺苷受体激活和腺苷受体数增多是腺苷对缺血心肌保护作用的基础.

AIM To investigate the pathological changes of liver tissue after acute ischemic injury and the effect of bupleurum polyclonum on such damage in rats. METHODS Rat hepatic portal blockage model was established. The pathologic changes were observed dynamically by light microscopy and electron microscopy after the liver ischemic injury in bupleurum polyclonum feeding group (BPG, n = 24) and generally feeding group (GFG, n = 24).RESULTS On the first day after operation, the rat s hepatocytes showed...

AIM To investigate the pathological changes of liver tissue after acute ischemic injury and the effect of bupleurum polyclonum on such damage in rats. METHODS Rat hepatic portal blockage model was established. The pathologic changes were observed dynamically by light microscopy and electron microscopy after the liver ischemic injury in bupleurum polyclonum feeding group (BPG, n = 24) and generally feeding group (GFG, n = 24).RESULTS On the first day after operation, the rat s hepatocytes showed severe retrograde degeneration, and the changes of endothelial cells were found with enlargement of the foramen between endothelial cells within the liver sinusoid and destruction in endothelial layers. On the 4th day after operation, granule changes and glycogen granulocyte reduction and chromatolysis were found in mitochondria of hepatocytes of the generally feeding group. But during this period, the specific structure of hepatocyte membrana such as desmosome and microvilli within the cholangiole could be viewed. On the 7th day after operation, the hepatocytes remained almost normal in the bupleurum polyclonum feeding group, and the changes of mitochondrion and rough neoplasmic reticulum were severe in the generally feeding group, including declination of mitochondrial matrix.CONCLUSION Bupleurum polyclonum can promote hepatocyte regeneration, restore liver injury. This result confirms the effect of bupleurum polyclonum on liver ischemic injury and establishes the pathological foundation for application of bupleurum polyclonum during perioperation.

目的 研究大鼠肝脏缺血性损伤后肝组织的病理学改变,以及柴胡煎剂的治疗作用。 方法 建立大鼠肝门完全阻断的模型,观察肝脏缺血性损伤后柴胡组和普食组在不同的时间阶段光镜和电镜下肝组织的病理学改变。 结果 电镜观察发现,术后1d各组肝窦内皮细胞孔隙加大,内皮破坏,内皮之间可见孔道,内皮细胞核内染色质浓聚,核膜仍完整;肝细胞肿胀,线粒体明显肿胀,基质变化,粗面内质网肿胀,脱颗粒,粗面内质网增多,细胞内糖原减少,细胞内溶酶体增多。细胞膜特化部分如桥粒、毛细胆管区微绒毛有轻微破坏。术后4d普食组肝窦内皮细胞孔隙大,内皮细胞核内染色质浓集于核膜;肝细胞肿胀,线粒体肿胀,基质密度变淡,内嵴结构模糊;粗面内质网排列不规则,脱颗粒,细胞膜破裂,肿胀变性的细胞器游离于胞外。柴胡组肝细胞轻度肿胀,核形态规则,出现吞饮小泡,肝细胞线粒体轻度肿胀,结构模糊,部分粗面内质网轻度扩张,糖原颗粒减少,可见溶酶体及脂滴,内皮膜欠光滑,基底部与肝细胞膜联系欠紧密。术后7d普食组肝细胞仍见轻度肿胀,线粒体轻度肿胀,结构模糊,基质变化,其内嵴变短,膜结构欠清楚;粗面内质网排列欠规则,糖原颗粒较少,可见少量溶酶体及脂滴。内膜欠完整,基底部与肝细胞联系欠...

目的 研究大鼠肝脏缺血性损伤后肝组织的病理学改变,以及柴胡煎剂的治疗作用。 方法 建立大鼠肝门完全阻断的模型,观察肝脏缺血性损伤后柴胡组和普食组在不同的时间阶段光镜和电镜下肝组织的病理学改变。 结果 电镜观察发现,术后1d各组肝窦内皮细胞孔隙加大,内皮破坏,内皮之间可见孔道,内皮细胞核内染色质浓聚,核膜仍完整;肝细胞肿胀,线粒体明显肿胀,基质变化,粗面内质网肿胀,脱颗粒,粗面内质网增多,细胞内糖原减少,细胞内溶酶体增多。细胞膜特化部分如桥粒、毛细胆管区微绒毛有轻微破坏。术后4d普食组肝窦内皮细胞孔隙大,内皮细胞核内染色质浓集于核膜;肝细胞肿胀,线粒体肿胀,基质密度变淡,内嵴结构模糊;粗面内质网排列不规则,脱颗粒,细胞膜破裂,肿胀变性的细胞器游离于胞外。柴胡组肝细胞轻度肿胀,核形态规则,出现吞饮小泡,肝细胞线粒体轻度肿胀,结构模糊,部分粗面内质网轻度扩张,糖原颗粒减少,可见溶酶体及脂滴,内皮膜欠光滑,基底部与肝细胞膜联系欠紧密。术后7d普食组肝细胞仍见轻度肿胀,线粒体轻度肿胀,结构模糊,基质变化,其内嵴变短,膜结构欠清楚;粗面内质网排列欠规则,糖原颗粒较少,可见少量溶酶体及脂滴。内膜欠完整,基底部与肝细胞联系欠紧密,柴胡组肝细胞未见肿胀,基本恢复到正常形态与结构,?

HQTYY,a compound prescription wich mainly consisted with Radix As-tragali,Radix Salviae Miltiorrhizae,Fructus Trichosanthis and Bulbus Allii Macrostemi,is often used to treat coronary heart diseases in clinic.The present study was undertaken to investigate the effects of HQTYY on hyperlipemia and pituitrin induced acute myocardial ischemia in rats.Methods:The male Wistar rast were di-vided into four groups.They were perfusated with adipose emulsion (1 ml/100g)or/and injected with pituitrin (0.7u/100g) in intraperitoneal...

HQTYY,a compound prescription wich mainly consisted with Radix As-tragali,Radix Salviae Miltiorrhizae,Fructus Trichosanthis and Bulbus Allii Macrostemi,is often used to treat coronary heart diseases in clinic.The present study was undertaken to investigate the effects of HQTYY on hyperlipemia and pituitrin induced acute myocardial ischemia in rats.Methods:The male Wistar rast were di-vided into four groups.They were perfusated with adipose emulsion (1 ml/100g)or/and injected with pituitrin (0.7u/100g) in intraperitoneal one time a day respec-tively.The HQTYY(1ml/100g)was administered in the treatment group in the mean time.At the eighth day,the ECG,some serum parameters and the variances of my-ocardial structure were detected and comparted.Results:The TG,LDL Contents in hyperlipemia control group were higher than those in normal control group,whereas the SOD was decreased significanly (P<0.01~0.001).The parameters above mentioned were aggravated when pituitrin was used.In addition,the HDL decreased and LPO.CK-MB and ST segment increased in this group (P<0.05~0.001).In contrast to this group,the TG,LDL,CK-MB were relieved and the HDL was a rel-atively high when administraten HQTYY(P<0.05~0.001).And the contents of SOD and LPO and the ST segment were similar as the hyperlipemia control group (P<0.05).Besides,the present study indicated that the injury of myocardial cells was alleviated in HOTYY group identified by microscope.Conclusion:The acute my-ocardial ischemia induced by pituitrin can deteriorate the hyperlipemia and can in-crease the production of the oxygen free radicals in the body.The HQTYY can reg-ulate the lipid metabolism,scavenge the oxygen free radicals and protect the my-ocardium from the acute ischemic injury caused by pituitrin.

目的黄芪痰瘀饮是本院临床治疗气虚血瘀、痰浊内阻型冠心病的常用自拟方,本研究利用大鼠实验模型,进一步观察了药物对高脂血症并急性心肌缺血的作用。方法实验分4组,模型组大鼠灌饲脂肪乳剂1ml/100g腹腔注射垂体后叶素Pit0.7u/100g药物组同时灌饲黄芪痰瘀饮1ml/100g正常对照组及高脂对照组予等量生理盐水对应给药,每日1次,第8d观测心电图变化、血清生化指标及心肌结构变化。结果高脂对照组与正常对照组相比血清甘油三酯TG、低密度脂蛋白LDL明显升高,超氧化物歧化酶SOD含量明显降低P<0.01~0.001;高脂加Pit组与高脂对照组相比TG、LDL进一步增高,SOD含量进一步下降,高密度脂蛋白HDL亦明显下降,过氧化脂质LPO、肌酸激酶同功酶MBCK-MB、ST段显著升高P<0.05~0.001;黄芪痰瘀饮组与高脂加Pit组相比TG、LDL、CK-MB较低,HDL较高P<0.05~0.001,而SOD、LPO、ST段变化与单纯高脂对照组相比无显著性差异P>0.05,光镜下见黄芪痰瘀饮组心肌受损程度轻于高脂加Pit组。结论Pit致急性心肌缺血可以恶化高脂血症,并使机体内氧自由基生成增多;黄芪痰瘀饮具有调脂、...

目的黄芪痰瘀饮是本院临床治疗气虚血瘀、痰浊内阻型冠心病的常用自拟方,本研究利用大鼠实验模型,进一步观察了药物对高脂血症并急性心肌缺血的作用。方法实验分4组,模型组大鼠灌饲脂肪乳剂1ml/100g腹腔注射垂体后叶素Pit0.7u/100g药物组同时灌饲黄芪痰瘀饮1ml/100g正常对照组及高脂对照组予等量生理盐水对应给药,每日1次,第8d观测心电图变化、血清生化指标及心肌结构变化。结果高脂对照组与正常对照组相比血清甘油三酯TG、低密度脂蛋白LDL明显升高,超氧化物歧化酶SOD含量明显降低P<0.01~0.001;高脂加Pit组与高脂对照组相比TG、LDL进一步增高,SOD含量进一步下降,高密度脂蛋白HDL亦明显下降,过氧化脂质LPO、肌酸激酶同功酶MBCK-MB、ST段显著升高P<0.05~0.001;黄芪痰瘀饮组与高脂加Pit组相比TG、LDL、CK-MB较低,HDL较高P<0.05~0.001,而SOD、LPO、ST段变化与单纯高脂对照组相比无显著性差异P>0.05,光镜下见黄芪痰瘀饮组心肌受损程度轻于高脂加Pit组。结论Pit致急性心肌缺血可以恶化高脂血症,并使机体内氧自由基生成增多;黄芪痰瘀饮具有调脂、对抗氧自由基、抗Pit致急性心肌缺血性损伤的作用。

 
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