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ischemic     
相关语句
  缺血
     Adenovirus-mediated gene transfer of vascular endothelial growth factor B induces angiogenesis in chronic ischemic myocardium
     腺病毒介导血管内皮生长因子B基因转染慢性缺血心肌血管新生的研究
短句来源
     Involvement of κ-Opioid Receptor in Ischemic Preconditioning and the Underlying Mechanism
     κ-阿片肽受体参与心肌缺血预处理的保护作用及其机制的研究
短句来源
     Mechanism Underlying the Cardioprotection of κ-opioid Receptor in Ischemic Preconditioning and Receptor Tolerance in the Rat Cardiomyocytes
     κ-阿片受体参与心肌缺血预处理保护作用及阿片受体耐受机制的研究
短句来源
     Protective Effect of Ischemic Preconditioning on the Hepatic Ischemia-Reperfusion and Lung Injury in Rats
     大鼠肝脏缺血预处理对肝脏及肺脏保护作用
短句来源
     The Study of Ischemic Pretreatment as well as Cardioprotection Function and Mechanism by using FFDSF
     复方丹参方预处理加强缺血预适应心肌保护作用及机制研究
短句来源
更多       
  缺血性
     INVOLVEMENT OF ENDOTHELIN-1 MECHANISM IN ACUTE ISCHEMIC ARRHYTHMIA
     急性缺血性心律失常的内皮素-1机制研究
短句来源
     Effects of Caspase-3, Calpain and Their Inhibitors on Ischemic Neuronal Damage in Rats
     Caspase-3与calpain在缺血性脑损伤中的作用及治疗干预的实验研究
短句来源
     Clinical Study on the Insulin Resistance of Ischemic Cerebrovascular Disease with Acupuncture
     针刺治疗缺血性脑血管病胰岛素抵抗的临床研究
短句来源
     The Effect of AQP4 on Ischemic Cerebral Edema
     水通道蛋白4在缺血性脑水肿中的作用机制研究
短句来源
     The Experimental Study of HuangJiao Grain on Acute Cerebral Ischemic Neuronal Apoptosis on Rats
     黄角颗粒抗大鼠急性缺血性神经细胞凋亡及其机制研究
短句来源
更多       
  脑缺血
     Protection by Monosialoganglionside (GM1) Against Cerebral Ischemic Injury and Its Mechanisms in Rats
     神经节苷脂GM1对大鼠脑缺血的保护作用及其机制的研究
短句来源
     Study of the Changes in NF-κ Bp65, I-κ B_α and COX-2 Following Focal Cerebral Ischemic Reperfusion in Rats
     NF-κ Bp65,I-κ B_α及COX-2在大鼠脑缺血再灌注损伤中的作用
短句来源
     Protection and Mechanisms by Aminoguanidine on Cerebral Ischemic Injury in Rats
     氨基胍对大鼠脑缺血的保护作用及其机制的研究
短句来源
     p38MAPK Participates in Brain Ischemic Tolerance Induced by Limb Ischemic Preconditioning and the Possible Underlying Mechanisms in Rats
     p38MAPK参与肢体缺血预处理诱导的大鼠脑缺血耐受及其机制初探
短句来源
     Neuroprotective Effect and Mechanisms of (-)clausenamide on Cerebral Ischemic Injury and APP Transgenic Mice
     (-)黄皮酰胺对脑缺血损伤和APP转基因小鼠的保护作用及机制
短句来源
更多       
  血性
     INVOLVEMENT OF ENDOTHELIN-1 MECHANISM IN ACUTE ISCHEMIC ARRHYTHMIA
     急性缺血性心律失常的内皮素-1机制研究
短句来源
     Effects of Caspase-3, Calpain and Their Inhibitors on Ischemic Neuronal Damage in Rats
     Caspase-3与calpain在缺血性脑损伤中的作用及治疗干预的实验研究
短句来源
     Clinical Study on the Insulin Resistance of Ischemic Cerebrovascular Disease with Acupuncture
     针刺治疗缺血性脑血管病胰岛素抵抗的临床研究
短句来源
     The Effect of AQP4 on Ischemic Cerebral Edema
     水通道蛋白4在缺血性脑水肿中的作用机制研究
短句来源
     The Experimental Study of HuangJiao Grain on Acute Cerebral Ischemic Neuronal Apoptosis on Rats
     黄角颗粒抗大鼠急性缺血性神经细胞凋亡及其机制研究
短句来源
更多       

 

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      ischemic
    Activation of δ2 ORs (DSLET, 0.5 mg/kg) has no effect on the incidence rate of ischemic and reperfusion arrhythmias.
          
    Choline succinate administration significantly improved memory and learning in ischemic rats and prevented the ischemia-induced decrease in the cerebral level of N-acetylaspartate.
          
    Thus, choline succinate demonstrated a neuroprotective effect in conditions of ischemic brain injury.
          
    Allopurinol, a competitive inhibitor of xanthine oxidase, was found to have a protective effect on ischemic myocardium.
          
    Activity of acidic sphingomyelinase initially decreased (during 15-30 min ischemia) but then increased (after 1 h of ischemic injury).
          
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    Cardiac output was determined according to Fick's principle, while renaI blood flow (RBF) and glomerular filtration rate (GFR) were measured from the clearances of PAH and creatinine. One hour after an i.v. injection of guanethidine 5 mg/kg, normal dogs showed a very slight hypotension, which was relatively more noticeable in renal hypertensive dogs. The cardiac output, stroke volume, and ventricular work tended to decrease tn normotensive dogs, but tended to augment in hypertensive dogs. These alterations,...

    Cardiac output was determined according to Fick's principle, while renaI blood flow (RBF) and glomerular filtration rate (GFR) were measured from the clearances of PAH and creatinine. One hour after an i.v. injection of guanethidine 5 mg/kg, normal dogs showed a very slight hypotension, which was relatively more noticeable in renal hypertensive dogs. The cardiac output, stroke volume, and ventricular work tended to decrease tn normotensive dogs, but tended to augment in hypertensive dogs. These alterations, however, were statistically insignificant. The total peripheral resistance was not much influenced by guanethidine in normal dogs, yet markedly diminished in hypertensive dogs. Diuresis was evident during the 1-hour postmedication period in both models. In hypertensive dogs, i.v. administrations of guanethidine caused a conspicuous rise of RBF and GFR, but a great reduction of the renal vascular resistance. In normal rats, following an i.p. injection of 20 mg/kg, the circulating blood volume (studied with I~(131)-labeled serum protein) exhibited a slight but non-significant increase within 3 hours, and returned to the original level at 24 hours. No significant change was found in DOCA-treated rats. Normal rats receiving guanethidine revealed an increase of blood volumes in all organs, especially spleen and kidney. These results demonstrate that the hypotensive action of guanethidine is not via the reduction of blood volume, but by way of a vasodilator action, which particularly amends the ischemic state of kidney and thus alleviates the pathologic process of renal hypertension.

    本文用正常血压及腎型高血压狗研究胍乙啶对心和腎的血流动力作用,并用大白鼠試驗其对循环及器官血容量的影响。根据Fick氏原則測定心輸出量,同时从腎脏对于对氨基馬尿酸及肌酐的清除率計算腎血流量及腎小球滤过率。靜脉注射胍乙啶5毫克/公斤1小时后,正常狗血压略有降低,高血压狗降压則較为明显。胍乙啶对正常血压狗的心輸出量、心搏量及心室作功量有減 低的趋向,而对腎型高血压狗則略有增加,但均不显著。胍乙啶不影响正常狗的外周血管阻力,而能显著降低腎型高血压狗的总外周阻力,扩张其外周血管。注射胍乙啶后,正常血压及腎型高血压狗的尿量增加均非常显著。腎型高血压狗的腎小球滤过率及腎血流量都非常显著地低于正常狗,腎血管阻力則大大地高于正常狗,靜脉注射胍乙啶后,滤过率及血流量均明显增加,而血管阻力則大大降低。正常大白鼠腹腔注射胍乙啶20毫克/公斤后,3小时內循环血量略有增加,但不显著,6小时后开始恢复,2斗小时后回至原水平。对注射DOCA的大白鼠的循环血量則沒有明显影响。正常大白鼠注射胍乙啶后,各器官及組織內合血量普遍有增加趋势,其中以脾及腎的血容量增加最为明显,說明胍乙啶对这些部位的血管有扩张作用。上述資料証明:胍乙啶的降压作用并非通...

    本文用正常血压及腎型高血压狗研究胍乙啶对心和腎的血流动力作用,并用大白鼠試驗其对循环及器官血容量的影响。根据Fick氏原則測定心輸出量,同时从腎脏对于对氨基馬尿酸及肌酐的清除率計算腎血流量及腎小球滤过率。靜脉注射胍乙啶5毫克/公斤1小时后,正常狗血压略有降低,高血压狗降压則較为明显。胍乙啶对正常血压狗的心輸出量、心搏量及心室作功量有減 低的趋向,而对腎型高血压狗則略有增加,但均不显著。胍乙啶不影响正常狗的外周血管阻力,而能显著降低腎型高血压狗的总外周阻力,扩张其外周血管。注射胍乙啶后,正常血压及腎型高血压狗的尿量增加均非常显著。腎型高血压狗的腎小球滤过率及腎血流量都非常显著地低于正常狗,腎血管阻力則大大地高于正常狗,靜脉注射胍乙啶后,滤过率及血流量均明显增加,而血管阻力則大大降低。正常大白鼠腹腔注射胍乙啶20毫克/公斤后,3小时內循环血量略有增加,但不显著,6小时后开始恢复,2斗小时后回至原水平。对注射DOCA的大白鼠的循环血量則沒有明显影响。正常大白鼠注射胍乙啶后,各器官及組織內合血量普遍有增加趋势,其中以脾及腎的血容量增加最为明显,說明胍乙啶对这些部位的血管有扩张作用。上述資料証明:胍乙啶的降压作用并非通过循环血量的減少,而是由于外周血管的扩张所致。胍乙啶能扩张腎血管,改善腎缺血状态,从而緩解腎型高血压的病理生理过程。

    Thirteen adult guinea-pigs were divided into 3 groups:2 as normal controls;6 and 5 being treated with streptomycin sulphate 200 and 400mg per kilo body weight res- pectively for 21—60 days.The vestibular and auditory functions were tested.Their brains were prepared for Bielschowsky and Nissl sections.Microscopic examination re- vealed the following facts. Vascular disturbances prevail in the nervous system.The blood vessels are crumpled with concommittent perivascular edema.The adjacent nervous tissue shows...

    Thirteen adult guinea-pigs were divided into 3 groups:2 as normal controls;6 and 5 being treated with streptomycin sulphate 200 and 400mg per kilo body weight res- pectively for 21—60 days.The vestibular and auditory functions were tested.Their brains were prepared for Bielschowsky and Nissl sections.Microscopic examination re- vealed the following facts. Vascular disturbances prevail in the nervous system.The blood vessels are crumpled with concommittent perivascular edema.The adjacent nervous tissue shows ischemic softening and the nerve fibres become demyelinated. The intoxicated nerve cells are generally dehydrated and shrunken often with eccen- tricity of nuclei and chromophilic lumps.Gliosis and neurophagosis are common. The vestibular and cochlear systems of the eighth or stato-acoustic nerve exhibit intoxicative changes in the 2 groups of animals.On the peripheral as well as the central side,the degeneration of the vestibular structures supercedes that of the cochlear system. The site and nature of the intoxication are much alike in the light and heavy-dose groups,yet the latter shows a higher severity. The degenerative alterations appear simultaneously in the perpheral and central struc- tures.A question of primacy in intoxication—peripheral or central—is not existent. There is a chain of structures on the peripheral and central sides of the stato-acoustic system;their degeneration does not proceed along the conduction path,nor the degree of intoxication varies with their relative positions on the conduction scale.The peri- pheral and central units get intoxicated independently. Besides the stato-acoustic structures streptomycin afflicts other sensory(e.g.trige- minal) and motor systems,the viscero-motor in particular.Streptomycin intoxication is general in nature,yet some structures are especially sensitive to it. The relative vulnerability to streptomycin of the nervous structures is apparently conditioned by their chemical constitution. Streptomycin injuries higher brain parts which are mainly motor,especially viscero- motor.The diencephalic viscero-motor nuclei,the striate complex and the visceral cor- tex are excessively disintegrated.The extensive intoxicative manifestations have a neurological basis. The toxin of streptomycin affects the entire nervous system and hence the whole bodily mechanisms.Its medical application calls for a meticulous consideration with respect to the patient's sensitivity to the antibiotic,the size of the dose and the length of the therapeutic course.

    十三个成长的豚鼠分为三粗,2个作正常对照,此外6个和5个每日分别注射链霉秦硫酸盐,一公斤体重200和400毫克,共经21至60天。未了,豚鼠都经过平衡和听觉的测验。各脑分别染制Nissl和Bielschowsky切片。显微镜的检查得到以下的结果。神经系中普见血管的病变。血管塌陷,管外间质水肿。邻近的神经组织失血软化。神经纤维表现髓鞘溶解。中毒的神经细胞脱水萎缩,常见胞核偏位,染色质偏聚、结块。也时有神经胶质增生和神经吞噬现象。二组豚鼠在位听神经的前庭系和耳蜗系都有中毒的征象。在周缘部和中枢部,前庭系各极结构的病变,与耳蜗系相较,更为严重。在注射轻剂和重剂的二组豚鼠,神经系中毒的部位和性质是相似的,但重剂组的病变程度较高。在位听系,中毒的病变同时见于周缘部和中枢部。中毒的第一性的问题——在周缘, 抑在中枢——是不存在的。周缘和中枢各有一系结构,病变的表现不沿神经传导的路线;病变的轻重也不随路线上地位的高低。周缘和中枢的各项结构是各自中毒的。链霉素不仅毒害位听神经一系,而更损伤其它感觉系(如三叉神经系)和运动系——特是内脏运动系——的结构。链霉素中毒是一般性的,但有些结构特易感受它的毒害。在各级结构中,神经细胞的...

    十三个成长的豚鼠分为三粗,2个作正常对照,此外6个和5个每日分别注射链霉秦硫酸盐,一公斤体重200和400毫克,共经21至60天。未了,豚鼠都经过平衡和听觉的测验。各脑分别染制Nissl和Bielschowsky切片。显微镜的检查得到以下的结果。神经系中普见血管的病变。血管塌陷,管外间质水肿。邻近的神经组织失血软化。神经纤维表现髓鞘溶解。中毒的神经细胞脱水萎缩,常见胞核偏位,染色质偏聚、结块。也时有神经胶质增生和神经吞噬现象。二组豚鼠在位听神经的前庭系和耳蜗系都有中毒的征象。在周缘部和中枢部,前庭系各极结构的病变,与耳蜗系相较,更为严重。在注射轻剂和重剂的二组豚鼠,神经系中毒的部位和性质是相似的,但重剂组的病变程度较高。在位听系,中毒的病变同时见于周缘部和中枢部。中毒的第一性的问题——在周缘, 抑在中枢——是不存在的。周缘和中枢各有一系结构,病变的表现不沿神经传导的路线;病变的轻重也不随路线上地位的高低。周缘和中枢的各项结构是各自中毒的。链霉素不仅毒害位听神经一系,而更损伤其它感觉系(如三叉神经系)和运动系——特是内脏运动系——的结构。链霉素中毒是一般性的,但有些结构特易感受它的毒害。在各级结构中,神经细胞的化学合成决定它们反应链霉素的灵钝和轻重。链霉素伤害高级的脑部,这多属运动性,特是内脏运动性。间脑的内脏性核团、纹状体簇和内脏性皮质中毒特别剧烈。链霉素中毒症状广泛,这是有神经基础的。链霉素的毒质伤害全神经系,也影响全身;为医疗使用这个抗菌素,关于患者对此药的敏感,剂量和疗程是要慎重考虑的。

    A long lasting change in EKG of ischemic nature characterized by depressedST segment could be provoked by electrical stimulation of the dorsal medialhypothalamic nucleus and the medial margin of the optic tract in anesthetizedrabbits.The stimulation employed consisted of 5—8 trains of square wave pulses.Each train was 5 minutes in duration and separated by an interval of 1—3minutes.Each square pulse was 0.2 msec in width,50 Hz,0.8—1.6 mA forweak stimulation or 4—8 mA for strong stimulation.Of the 42 cases...

    A long lasting change in EKG of ischemic nature characterized by depressedST segment could be provoked by electrical stimulation of the dorsal medialhypothalamic nucleus and the medial margin of the optic tract in anesthetizedrabbits.The stimulation employed consisted of 5—8 trains of square wave pulses.Each train was 5 minutes in duration and separated by an interval of 1—3minutes.Each square pulse was 0.2 msec in width,50 Hz,0.8—1.6 mA forweak stimulation or 4—8 mA for strong stimulation.Of the 42 cases tested,32revealed remarkable changes in EKG,after the first train of weak hypothalamicstimulation.Among them,15 showed marked ST depression,7 ST elevation,5T-wave inversion or flattening and 3 T-wave peaking.As the stimulating trainsincreased in number and strength all the EKGs were eventually manifested bypersistent depression of ST segemnt.It was found that the abnormal manifesta-tion of EKG could be partially relieved by spinal transection at C_2 level andaugmented after vagotomy.Moreover,the abnormality in EKG induced by thehypothalamic stimulation could be improved by administration of antianginaldrugs such as inhalation of amyl nitrite and intravenous injection of chrysanthe-mum sinense solution.It is suggested that the electrocardiographic changesinduced by the hypothalamic stimulation are ischemic in nature and can betaken as an index of the animal model to essay the effeciency of variousantianginal drugs.

    (1)以两支尖端裸露约0.5—0.8毫米的绝缘不锈钢针同时通电刺激麻醉家兔的右侧下丘脑背内侧核与视径两部位,方波刺激参数为波宽0.2毫秒、频率每秒50次,强度分为两级,弱刺激0.8—1.6毫安,强刺激4—8毫安,每次刺激5分钟,间隔1—3分钟,经5—8次刺激(多数为2次弱刺激、3次强刺激)后可以获得较持久而稳定的以 ST段压低为主要特征的缺血性心电波形。(2)在42例急性实验中,32例经一次弱刺激5分钟后即表现明显的心电图变化,其中15例呈明显 ST 段压低,7例 ST 段抬高,5例先表现 T 波倒置或变平,3例先表现 T 波增高。随着刺激次数增多与强度增强,最后均出现持久而稳定的 ST 段压低。 (3)切断脊髓使 ST 段压低与 T 波倒置的程度减轻,切断迷走神经见 T 波倒置加深。(4)吸入亚硝酸异戊酯与注射菊花液等能改善 ST 段压低的程度,故这种缺血性心电变化可用作测试抗心绞痛药物的一种动物模型。

     
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