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acute myocardial ischemic damage
相关语句
  急性心肌缺血性损伤
     AIM: To observe the activation of peroxisome proliferate-activated receptor α(PPARα) by fenofibrate of agonists of PPARα after pre-application, and the effects on tumor necrosis factor alpha (TNF-α) in acute myocardial ischemic damage rats.
     目的观察预先应用过氧化物酶体增殖物激活受体α的激动剂非诺贝特活化过氧化物酶体增殖物激活受体α,对急性心肌缺血性损伤大鼠血清肿瘤坏死因子α的影响。
短句来源
     But it was higher in the fenofibrate group than that in the isoproterenol group (P < 0.01=. CONCLUSION: After activation the PPARα takes part in the inflammatory reaction in acute myocardial ischemic damage and distinctly inhibit the expression of TNF-α, which indicates that the fenofibrate has certain protective effect on myocardial ischemia.
     但非诺贝特组高于异丙肾上腺素组(P<0.01)。 结论过氧化物酶体增殖物激活受体α活化后参与急性心肌缺血性损伤中的炎症反应,显著抑制肿瘤坏死因子α表达。
短句来源
  “acute myocardial ischemic damage”译为未确定词的双语例句
     Relationship between the activation of peroxisome proliferate-activated receptor alpha and the expression of tumor necrosis factor alpha in acute myocardial ischemic damage
     急性心肌缺血损伤中过氧化物酶体增殖物激活受体α活化与肿瘤坏死因子α表达的关系
短句来源
     ② After the last gastric perfusion for 1 hour the rats in the isoproterenol group and fenofibrate group were given 5 mg/kg isoproterenol with intraperitoneal injection to replicate acute myocardial ischemic damage models.
     ②末次灌胃后1h异丙肾上腺素组和非诺贝特组给予异丙肾上腺素5m g/kg腹腔注射复制急性心肌缺血损伤模型;
短句来源
     EFFECT OF ELECTRO-ACUPUNCTURE ON THE SEGMENT LENGTH OF THE MYOCARDIUM AND THE LEFT INTRAVENTRICULAR PRESSURE-LENGTH VECTOR LOOP DURING EXPERIMENTAL ACUTE MYOCARDIAL ISCHEMIC DAMAGE
     电针对心肌缺血性损伤时心肌节段长度和左室内压——长度环的影响
短句来源
  相似匹配句对
     Myocardial ischemic damage after acute stroke
     卒中后的心肌缺血样损伤
短句来源
     Effect of Laser Acupuncture at Neiguan Point on Acute Ischemic Myocardial Damage in Rabbits
     激光针内关等穴位对家兔急性缺血性心肌损伤的影响
短句来源
     Laboratory Progress in Ischemic Myocardial Damage Detection
     缺血性心脏病的实验室诊断进展
短句来源
     Myocardial damage caused by acute organophosphoms poisoning
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短句来源
     Effects of Ischemic Preconditioning on Acute Myocardial Infarction
     心肌缺血预适应对急性心肌梗塞的影响
短句来源
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AIM: To observe the activation of peroxisome proliferate-activated receptor α(PPARα) by fenofibrate of agonists of PPARα after pre-application, and the effects on tumor necrosis factor alpha (TNF-α) in acute myocardial ischemic damage rats. METHODS: The experiment was performed at the Institute of Keshan Disease, Harbin Medical University from June 2004 to May 2005. Thirty healthy pure male Wistar rats were selected and assigned randomly into isoproterenol group, fenofibrate group and normal control group...

AIM: To observe the activation of peroxisome proliferate-activated receptor α(PPARα) by fenofibrate of agonists of PPARα after pre-application, and the effects on tumor necrosis factor alpha (TNF-α) in acute myocardial ischemic damage rats. METHODS: The experiment was performed at the Institute of Keshan Disease, Harbin Medical University from June 2004 to May 2005. Thirty healthy pure male Wistar rats were selected and assigned randomly into isoproterenol group, fenofibrate group and normal control group with 10 rats in each group. ① The fenofibrate was dissolved into 30 g/L gum acacia to make suspension. The rats in the fenofibrate group were treated with 80 mg/kg fenofibrate with gastric perfusion. Those in the other two groups were given 30 g/L gum acacia at the same volume with gastric perfusion, once a day for 7 days. ② After the last gastric perfusion for 1 hour the rats in the isoproterenol group and fenofibrate group were given 5 mg/kg isoproterenol with intraperitoneal injection to replicate acute myocardial ischemic damage models. Those in the normal control group were given saline at the same volume with intraperitoneal injection. After injecting with isoproterenol for 24 hours, the serum and part of heart were gained after anesthesia. Concentration of TNF-α in serum was detected with enzyme-linked immunosorbent assay (ELISA). Expression of PPARα mRNA in myocardial tissue was tested with reverse transcription-polymerase chain reaction (RT-PCR). RESULIS: Thirty rats were involved in the result analysis. ① Concentration of TNF-α: It was higher in the isoproterenol group and fenofibrate group than that in the normal control group [(301.72±2.49),(164.29 ±3.60),(16.35±2.37)ng/L,P < 0.01]. But it was lower in the fenofibrate group than that in the isoproterenol group (P < 0.01). ② Expressive level of PPARα mRNA in myocardial tissue: It was lower in the isoproterenol group and fenofibrate group than that in the normal control group (0.735 5 ±0.045 5,0.886 3±0.032 2,0.926 7±0.031 9,P < 0.01). But it was higher in the fenofibrate group than that in the isoproterenol group (P < 0.01=. CONCLUSION: After activation the PPARα takes part in the inflammatory reaction in acute myocardial ischemic damage and distinctly inhibit the expression of TNF-α, which indicates that the fenofibrate has certain protective effect on myocardial ischemia.

目的观察预先应用过氧化物酶体增殖物激活受体α的激动剂非诺贝特活化过氧化物酶体增殖物激活受体α,对急性心肌缺血性损伤大鼠血清肿瘤坏死因子α的影响。方法实验于2004-06/2005-05在哈尔滨医科大学克山病研究所完成。取30只健康纯系雄性W istar大鼠随机分为异丙肾上腺素组、非诺贝特组和正常对照组3组,每组10只。①非诺贝特溶于30g/L阿拉伯树胶中制成混悬液,非诺贝特组给予非诺贝特80m g/kg灌胃,其他两组给予等量的30g/L阿拉伯树胶灌胃,1次/d,,共7d。②末次灌胃后1h异丙肾上腺素组和非诺贝特组给予异丙肾上腺素5m g/kg腹腔注射复制急性心肌缺血损伤模型;正常对照组给予等量的生理盐水腹腔注射。异丙肾上腺素注射24h,麻醉后取血清和部分心脏,用酶联免疫吸附实验测定血清中肿瘤坏死因子α的浓度,用反转录-聚合酶链反应测定心肌组织中过氧化物酶体增殖物激活受体αm RNA表达水平。结果30只大鼠进入结果分析。①血清中肿瘤坏死因子α的浓度异丙肾上腺素组和非诺贝特组高于正常对照组[(301.72±2.49),(164.29±3.60),(16.35±2.37)ng/L,P<0.01],但非诺贝特组低于异...

目的观察预先应用过氧化物酶体增殖物激活受体α的激动剂非诺贝特活化过氧化物酶体增殖物激活受体α,对急性心肌缺血性损伤大鼠血清肿瘤坏死因子α的影响。方法实验于2004-06/2005-05在哈尔滨医科大学克山病研究所完成。取30只健康纯系雄性W istar大鼠随机分为异丙肾上腺素组、非诺贝特组和正常对照组3组,每组10只。①非诺贝特溶于30g/L阿拉伯树胶中制成混悬液,非诺贝特组给予非诺贝特80m g/kg灌胃,其他两组给予等量的30g/L阿拉伯树胶灌胃,1次/d,,共7d。②末次灌胃后1h异丙肾上腺素组和非诺贝特组给予异丙肾上腺素5m g/kg腹腔注射复制急性心肌缺血损伤模型;正常对照组给予等量的生理盐水腹腔注射。异丙肾上腺素注射24h,麻醉后取血清和部分心脏,用酶联免疫吸附实验测定血清中肿瘤坏死因子α的浓度,用反转录-聚合酶链反应测定心肌组织中过氧化物酶体增殖物激活受体αm RNA表达水平。结果30只大鼠进入结果分析。①血清中肿瘤坏死因子α的浓度异丙肾上腺素组和非诺贝特组高于正常对照组[(301.72±2.49),(164.29±3.60),(16.35±2.37)ng/L,P<0.01],但非诺贝特组低于异丙肾上腺素组(P<0.01)。②心肌组织中过氧化物酶体增殖物激活受体αm RNA表达水平异丙肾上腺素组和非诺贝特组低于正常对照组(0.7355±0.0455,0.8863±0.0322,0.9267±0.0319,P<0.01);但非诺贝特组高于异丙肾上腺素组(P<0.01)。结论过氧化物酶体增殖物激活受体α活化后参与急性心肌缺血性损伤中的炎症反应,显著抑制肿瘤坏死因子α表达。提示非诺贝特对心肌缺血有一定保护作用。

 
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