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ischemic brain tissue
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  缺血侧脑组织
    Then stripping ischemic brain tissue on ice cubes after decapitation, homogenating, Detected by ELISA method to investigate the content of sICAM-1 in rats' blood and
    部分大鼠采血后断头处死在冰块上迅速取缺血侧脑组织,匀浆,用磷基转移片法检测
短句来源
    The Experimental Research on Neuroprotective Mechanism of Acupuncture Method in Focal Cerebral Ischemic RatsObjective: To observe the inflammatory reaction and morphologic changes in ischemic brain tissue, related changes of cytokine and adhesion molecule,and the effect of acupuncture method on focal cerebral ischemia in ratsMethods: (1) Use photochemical method inducing one-side middle cerebral artery occlusion in rats to make focal cerebral ischemia experimental model.
    针刺对局灶性脑缺血大鼠神经功能保护作用的机理研究目的:观察针刺治疗局灶性脑缺血模型大鼠血清与缺血侧脑组织炎症反应与形态学改变,以及在缺血半暗区部分与此相关的神经细胞因子、血液流变学以及溶栓作用变化,探讨针刺干预作用的机理研究。 方法:①采用光化学诱导法阻断大脑中动脉区造成大鼠局灶性脑缺血模型;
短句来源
    (3) Use morphologic method to observe the inflammatory reaction in ischemic brain tissue,especially the phenomena of adhesiveness and infiltration of the inflammatory cells.
    ③应用形态学方法观察缺血侧脑组织炎症反应,重点观察缺血半暗带炎性细胞的粘附及浸润现象;
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  “ischemic brain tissue”译为未确定词的双语例句
    Radioimmunoassay was applied to evaluate the PAF and TXB 2 (stable metabolite of TXA 2) levels in rat ischemic brain tissue. Results Compared with the sham operated control group,a great increase in the PAF concentrations in simple ischemia and 3 h,6 h,12 h,18 h reperfusion groups were observed.
    对应血栓素B2 值再灌注 3h增加 ,在 18h达高峰 ,两者分别于再灌注 2 4h和 36h降至对照组水平。
短句来源
    CONCLUSION: Blood-letting puncture on 12-well points of hand inhibits the increased NO content and NOS activity in ischemic brain tissue and alleviates the injury of free radical to brain tissue so that the focal brain ischemia of rats is protected.
    结论:“手十二井穴”刺络放血可抑制脑缺血后脑组织一氧化氮含量,一氧化氮合酶活性升高,减轻自由基对脑组织损伤,从而对大鼠局灶性脑缺血有保护作用。
短句来源
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  ischemic brain tissue
They also suggest that alkaline pH shifts that occur after blood reperfusion of ischemic brain tissue might be critical for the survival of cells.
      
Inhibition of excitatory neurotransmitters should therefore result in cytoprotection of ischemic brain tissue.
      
The release of the neurotransmitter, glutamate, and the activation of receptor operated calcium channels, may increase the degree of damage in ischemic brain tissue.
      
The results from our study suggest that this relation may also exist in vivo in ischemic brain tissue.
      
Cerebral blood vessels, atherosclerotic endothelium, and ischemic brain tissue are good targets of gene transfer.
      
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Objective To study the relationship between platelet activating factor(PAF) and arachidonic acid and observe the effects of PAF receptor antagonists kadsurenin mixture,kadsurenone,ginkgolide B on PAF and TXA 2 after focal cerebral ischemia reperfusion in rats.Methods Focal cerebral ischemia was induced by inserting a nylon suture into the right intracranial segment of internal carotid artery from external carotid artery to block the origin of middle cerebral artery. For reperfusion,the suture was pulled...

Objective To study the relationship between platelet activating factor(PAF) and arachidonic acid and observe the effects of PAF receptor antagonists kadsurenin mixture,kadsurenone,ginkgolide B on PAF and TXA 2 after focal cerebral ischemia reperfusion in rats.Methods Focal cerebral ischemia was induced by inserting a nylon suture into the right intracranial segment of internal carotid artery from external carotid artery to block the origin of middle cerebral artery. For reperfusion,the suture was pulled out to restore the blood flow to the ischemic brain.Senile Wistar rats were randomly devided into twelve groups:sham operated control group,simple ischemia for 90 min group,3 h,6 h,12 h,18 h,24 h,36 h,48 h reperfusion groups,and kadsurenin mixture,kadsurenone,ginkgolide B treated groups.In sham operated rats,the thread was inserted only 9 millimeter.Radioimmunoassay was applied to evaluate the PAF and TXB 2 (stable metabolite of TXA 2) levels in rat ischemic brain tissue.Results Compared with the sham operated control group,a great increase in the PAF concentrations in simple ischemia and 3 h,6 h,12 h,18 h reperfusion groups were observed.In contrast,the marked increase in the TXB 2 level was present after 3 h of reperfusion.The peak levels of PAF and TXB 2 were observed at 12 h and 18 h reperfusion,retuned to basal values at 24 h and 36 h respectively.However,pretreatment with three PAF receptor antagonists as mentioned above significantly alleviated the increase in PAF and TXB 2 levels at 12 h reperfusion.Conclusions It was considered that increase in TXA 2 might be closely related to PAF,which is involved in the progress of ischemic neuropathological damages.Two natural PAF receptorantagonists can reduce the elevation of PAF and TXA 2 and correct the disorder of arachidonic acid after cerebral ischemic reperfusion.

目的 研究海风藤新木脂素类成分等天然血小板活化因子 (PAF)受体拮抗剂对脑缺血后PAF及花生四烯酸(AA)代谢的作用影响 ,探讨内在关系及机制。方法 应用放免法测定大脑中动脉线栓闭塞再通不同时相大脑中动脉供血区顶叶皮质PAF、血栓素B2 浓度。结果 单纯缺血 90min时 ,PAF含量已显著高于对照组 ,再灌注 3h稍有回降 ,随即持续升高至 12h ;对应血栓素B2 值再灌注 3h增加 ,在 18h达高峰 ,两者分别于再灌注 2 4h和 36h降至对照组水平。海风藤新木脂素复合物、海风藤酮及银杏叶类制剂银杏内酯B均能明显抑制PAF和血栓素B2 的升高。结论 局灶性脑缺血再灌注后 ,PAF与AA协同参与了神经细胞损伤的发生及发展过程。两类天然PAF受体拮抗剂均可抑制脑缺血后PAF的过量生成、纠正AA代谢紊乱

BACKGROUND: Blood-letting puncture on 12-well points of hand is a kind of effective emergent approaches on cerebral apoplexy. It is testified in animal experiment that bleeding on 12-well points of hand can dilate cerebral vessels, enhance blood flow in brain, improve acute anoxic state in ischemic brain tissue and relieve acid toxin due to accumulation of lactate.OBJECTIVE: To explore the effects and mechanism of blood-letting puncture of 12-well points of hand nitric oxide (NO) contents and nitricoxide...

BACKGROUND: Blood-letting puncture on 12-well points of hand is a kind of effective emergent approaches on cerebral apoplexy. It is testified in animal experiment that bleeding on 12-well points of hand can dilate cerebral vessels, enhance blood flow in brain, improve acute anoxic state in ischemic brain tissue and relieve acid toxin due to accumulation of lactate.OBJECTIVE: To explore the effects and mechanism of blood-letting puncture of 12-well points of hand nitric oxide (NO) contents and nitricoxide synthase (NOS) activity after cerebral ischemia in rats.DESIGN: Randomized controlled animal experiment was designed.SETTING: Department of Physiology of Medical Institute of Xianning College.MATERIALS: The experiment was performed in Department of Physiology of Medical Institute of Xianning College from March 2003 to February 2004. Totally 84 Wistar rats were employed in the experiment, aged of 2 or 3 months, of either sex, body weighted (230±20) g and provided from Experimental Animal Center of Medical Institute of Xianning College.METHODS: Totally 84 rats were randomized into sham operation group, ischemia group and ischemia + bleeding group, 28 rats in each one. Modified Longa method3 was applied to prepare the model of embolism of cerebral middle artery in rat. In ischemia + bleeding group, after cerebral ischemia, blood-letting puncture was applied with three-edged needle on Shaoshang (LU11), Shangyang (LI1), Zhongchong (PC9), Guanchong (TE1), Shaochong (HT9) and Shaoze (SI1) in sequence firstly on the left foreleg, and then on the right one, corresponding to the analogy of 12-well points of hand of human. One blood drop was just required. NO content and NOS activity were assayed in 30 minutes, 1 hour, 2 hours and 4 hours of ischemia in brain tissue successively in each group.MAIN OUTCOME MEASURES: NO content and NOS activity in brain tissue in each group.RESULTS: ① NO content in 30 minutes, 1 hour, 2 hours and 4 hours of ischemia in ischemia group was (116.16±26.63), (118.94±24.47), (115.65±25.29) and (108.87±26.52) μmol/L successively and NOS activity was (507.22±92.52), (502.08±92.52), (510.71±96.63) and (495.29 ±88.41) μkat/L, which was higher significantly than the sham operation group (t=2.474-4.731, P < 0.05 or 0.001). ② In ischemia + bleeding group, NO content was (91.8±11.51), (93.55±13.88), (92.52±11.62) and (84.3±11.51) μmol/L successively and NOS activity was (337.6±88.41), (340.99±96.63), (344.48±84.3) and (337.6±90.46) μkat/L, indicating significant difference in comparison with ischemia group (t=2.199-3.507, P < 0.05-0.01).CONCLUSION: Blood-letting puncture on 12-well points of hand inhibits the increased NO content and NOS activity in ischemic brain tissue and alleviates the injury of free radical to brain tissue so that the focal brain ischemia of rats is protected.

背景:“手十二井穴”刺络放血疗法是治疗脑卒中的一种有效急救方法,动物实验证明“手十二井穴”刺络放血具有扩张脑血管,增加脑血流量,改善缺血区脑组织的急性缺氧状态,缓解乳酸堆积造成的酸中毒等作用。目的:探讨“手十二井穴”刺络放血对大鼠脑缺血后一氧化氮含量和一氧化氮合酶活性变化的影响及机制。设计:随机对照动物实验。单位:咸宁学院医学院生理教研室。材料:实验于2003-03/2004-02在咸宁学院医学院生理教研室完成。实验选用84只Wistar大鼠,鼠龄二三个月,雌雄兼用,体质量(230±20)g,由咸宁学院医学院实验动物中心提供。方法:将84只大鼠随机分为假手术组、缺血组、缺血+刺络放血组,每组28只。采用改良Longa法犤3犦制作大鼠大脑中动脉栓塞模型,缺血+刺络放血组在脑缺血后立即用三棱针按少商,商阳,中冲,关冲,少冲,少泽的顺序,先左前肢,后右前肢,点刺相当于人的“手十二井穴”解剖位置,使出一滴血,以不下滴为度。各组分别在缺血30min,1,2,4h取脑组织,测定一氧化氮含量和一氧化氮合酶活性。主要观察指标:各组大鼠脑组织一氧化氮含量和一氧化氮合酶活性。结果:①缺血组大鼠在缺血30min,1,2,4h一氧化...

背景:“手十二井穴”刺络放血疗法是治疗脑卒中的一种有效急救方法,动物实验证明“手十二井穴”刺络放血具有扩张脑血管,增加脑血流量,改善缺血区脑组织的急性缺氧状态,缓解乳酸堆积造成的酸中毒等作用。目的:探讨“手十二井穴”刺络放血对大鼠脑缺血后一氧化氮含量和一氧化氮合酶活性变化的影响及机制。设计:随机对照动物实验。单位:咸宁学院医学院生理教研室。材料:实验于2003-03/2004-02在咸宁学院医学院生理教研室完成。实验选用84只Wistar大鼠,鼠龄二三个月,雌雄兼用,体质量(230±20)g,由咸宁学院医学院实验动物中心提供。方法:将84只大鼠随机分为假手术组、缺血组、缺血+刺络放血组,每组28只。采用改良Longa法犤3犦制作大鼠大脑中动脉栓塞模型,缺血+刺络放血组在脑缺血后立即用三棱针按少商,商阳,中冲,关冲,少冲,少泽的顺序,先左前肢,后右前肢,点刺相当于人的“手十二井穴”解剖位置,使出一滴血,以不下滴为度。各组分别在缺血30min,1,2,4h取脑组织,测定一氧化氮含量和一氧化氮合酶活性。主要观察指标:各组大鼠脑组织一氧化氮含量和一氧化氮合酶活性。结果:①缺血组大鼠在缺血30min,1,2,4h一氧化氮含量分别为(116.16±26.63),(118.94±24.47),(115.65±25.29),(108.87±26.52)μmol/L,一氧化氮合酶活性分别为(507.22±92.52),(502.08±92.52),(510.71±96.63),(495.29±88.41)μkat/L,显著高于假手术组(t=2.474~4.731,P<0.05~0.001)。②缺血+刺络放血组一氧化氮含量分别为(91.8±11.51),(93.55±13.88),(92.52±11.62),(84.3±11.51)μmol/L,一氧化氮合酶活性分别为(337.6±88.41),(340.99±96.63),(344.48±84.3),(337.6±90.46)μkat/L,与缺血组比较差异有显著性意义(t=2,199~3.507,P<0.05~0.01)。结论:“手十二井穴”刺络放血可抑制脑缺血后脑组织一氧化氮含量,一氧化氮合酶活性升高,减轻自由基对脑组织损伤,从而对大鼠局灶性脑缺血有保护作用。

 
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