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brain ischemic damage
相关语句
  脑缺血性损害
     Objective To investigate the possible roles of endothelin? 1 (ET?1)and nitric oxide (NO) in the development of cerebral vasospasm(CVS) and related brain ischemic damage following subarachnoid hemorrhage (SAH).
     目的 :探讨内皮素 (ET) 1和一氧化氮 (NO)在蛛网膜下腔出血 (SAH)后脑血管痉挛 (CVS)及脑缺血性损害中的作用。
短句来源
  “brain ischemic damage”译为未确定词的双语例句
     Effects of Aminoguanidine on Blood Brain Barrier and Brain Ischemic Damage during Reperfusion of Cerebral Ischemia in Rats
     氨基胍对大鼠脑缺血再灌注损伤及血脑屏障的影响
短句来源
     Conclusion: Increase of ET1 concentrations in plasma and brain tissue plays an important important role in the development of acute CVS and related brain ischemic damage after SAH.
     结论 血浆及脑组织ET1增加在SAH后急性CVS及其脑缺血损害发生发展中起重要作用。
短句来源
     EXPERIMENTAL STUDY ON BRAIN ISCHEMIC DAMAGE
     尼莫地平对缺血性脑损害的实验研究
短句来源
     Study on the Molecular Mechanism of Brain Ischemic Damage by Cerebral Vasospasm the Effects of Tetrandrine in Rabbits
     实验性蛛网膜下腔出血脑血管痉挛后缺血性脑损害的发病机理及粉防己碱的干预作用研究
短句来源
     Conclusion: SEP is useful in the judgement of brain ischemic damage after SAH.
     结论 :SEP对SAH后脑缺血损伤的判断有重要意义。
短句来源
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  相似匹配句对
     EXPERIMENTAL STUDY ON BRAIN ISCHEMIC DAMAGE
     尼莫地平对缺血性脑损害的实验研究
短句来源
     Erythropoietinand Hypoxic-ischemic Brain Damage
     促红细胞生成素与缺氧缺血性脑损伤
短句来源
     Caspase and hypoxic ischemic brain damage
     半胱天冬酶与缺氧缺血性脑损伤
短句来源
     Study on pathogenesis of hypoxic-ischemic on brain damage
     缺氧缺血致脑损伤机理的研究
短句来源
     CONCLUSION: Nim protects the brain from ischemic damage.
     结论:Nim对缺血引起损伤的神经有保护作用。
短句来源
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Using a modified method of Pulsinelli's induction of brain ischemic damage in wistar rat by 4-vessel occlusion, calcium content in hippocampus was found significantly higher in ischemic group. Nimodipine (1 mg/kg) was injected intraperitoneally following brain ischemia, the calcium content in hippocampus had no significant difference between Nimodipine treated group and ischemic group.

本文将51只雄性Wistar大鼠随机分成假手术对照组、缺血组、缺血-尼莫地平组。采用改良Pulsinelli法建立鼠脑缺血模型,并经脑电图监测及组织病理学检查证实缺血模型是成功的。缺血-尼莫地平组的大鼠在夹闭颈总动脉造成鼠脑暂时性缺血的同时於腹腔内注射尼莫地平。比较对照组及暂时性缺血再灌注72小时后海马组织钙含量,用原子吸收分光光度计测定发现缺血组海马组织钙含量增高,但缺血-尼莫地平组海马组织钙含量与缺血组差异无显著性。

Previous studies had shown that dl-3-n -butylphthalide (NBP) could protect rat from cerebral ischemic damage subjected to middle cerebral artery occlusion. In order to clarify the mechanism of pharmacological action of NBP, the effects of NBP on contraction of rat isolated tail artery induced by KCl or norepinephrine (NE) were studied. The results show that NBP at the concentration of 100 or 500 μmol·L -1 competitively inhibited the contraction induced by NE and non-competitively inhibited the contractioninduced...

Previous studies had shown that dl-3-n -butylphthalide (NBP) could protect rat from cerebral ischemic damage subjected to middle cerebral artery occlusion. In order to clarify the mechanism of pharmacological action of NBP, the effects of NBP on contraction of rat isolated tail artery induced by KCl or norepinephrine (NE) were studied. The results show that NBP at the concentration of 100 or 500 μmol·L -1 competitively inhibited the contraction induced by NE and non-competitively inhibited the contractioninduced by KCl. The values of pA 2 and pD 2 'were 4.86 ±0.13 and 3.57±0.14 respectively. Compared with nimodipine (pD 2 '=8.50±0.20), NBP had weaker influence on voltage-dependent calcium channel. It is also shown that NBP at concentration of 100 μmol·L -1 inhibited the contraction induced by NE-dependent intracellular calcium, but NBP had no effect on contraction induced by extracellular calcium. The results suggest that the inhibiting action of NBP on intracellular calcium release initiated by NE in vascular smooth muscle may be responsible for the protective effect of NBP on brain ischemic damage.

丁基苯酞(NBP)对脑缺血损伤有保护作用,为探讨其作用机制,采用离体大鼠尾动脉环为标本,观察了NBP对KCl和去甲肾上腺素所致尾动脉收缩的影响,以及NBP与细胞内,外钙的关系.结果表明:NBP在大剂量时,能非竞争性及竞争性地抑制KCl及去甲肾上腺素引起的血管收缩.pD'2及pA2值分别为3.57±0.14及4.86±0.13,表明作用较弱.NBP100μmol·L-1对去甲肾上腺素的内源性钙收缩有抑制作用,而对外源性钙收缩无影响.说明NBP抑制内钙释放作用比对外钙的阻断作用强

Objective To investigate the secondary brain ischemic damage and the role that nitric oxide plays after subarachnoid hemorrhage (SAH).Methods Noncraniotomy models of SAH in Wistar rats were used to determine the dynamic changes of microregional cerebral blood flow and intracranial serum nitric oxide content within 24h. Diameter of basilar artery was also measured. Results Microregional cerebral blood flow reduced immediately after SAH,reaching its nadir at 1h,maintaining at a lower level within 24h(P<0.01)....

Objective To investigate the secondary brain ischemic damage and the role that nitric oxide plays after subarachnoid hemorrhage (SAH).Methods Noncraniotomy models of SAH in Wistar rats were used to determine the dynamic changes of microregional cerebral blood flow and intracranial serum nitric oxide content within 24h. Diameter of basilar artery was also measured. Results Microregional cerebral blood flow reduced immediately after SAH,reaching its nadir at 1h,maintaining at a lower level within 24h(P<0.01). Serum nitric oxide content decreased from 1h to 24hs after SAH (P< 0.01 ). Diameter of basilar artery reduced significantly 0. 5h after onset of SAH(P<0.01 ). Condusions Reduction of cerebral perfusion pressure,spasm of the cerebral arteries and microcirculatory disturbance may contribute to the decrease of microregional cerebral blood flow following SAN.Reduction of nitric oxide level may be one of the important factors that are responsible for cerebral vasospasm and disturbance of microcirculation.

目的探讨蛛网膜下腔出血(SAH)后继发性脑缺血损害及其一氧化氮(NO)的作用。方法应用非开颅性方法建立大鼠SAH模型,检测24h内脑微区血流量和颅内血清NO的动态改变,并测量基底动脉(BA)管径。结果SAH后脑微区血流量迅速降低,1h达最低值,24h内无明显恢复趋势(P< 0.01)。SAH后1h血清NO开始减低,井持续24h(P<0.01)。BA管径于SAH后明显缩小(P<0.01)。结论SAH时脑灌注压降低、脑血管痉挛及微循环异常均可能与脑血流量降低有关。NO减少是脑血管

 
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