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ketamine相关的网络例句

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与 ketamine 相关的网络例句 [注:此内容来源于网络,仅供参考]

We reported increases in locomotor activity with administration of ketamine in 22-, 35-, and 50-day-old mice and showed that the effects of ketamine diminish with age.

结果表明:使用氯胺酮可增加22、35和50日龄小鼠的运动器官的敏捷性,并证明了氯胺酮的作用随年龄的增长而降低;使用氯胺酮所导致的旋转与年龄的变化有关,但站立的减少与年龄无关,这种减少不依赖于小鼠的年龄

Plexus brachialis nerves block combined with ketamine propofol intravenous anesthesia used in the operation of children's arm can decrease the quantity of ketamine to reduce the uncomfortable response.In this way,the children's breath and circulation is more steadily during the anesthesia and operation.The parents and doctors'satisfactory are highly increased.

臂丛神经阻滞复合氯胺酮-丙泊酚静脉麻醉应用于小儿上肢手术,可减少氯胺酮用量从而减少其不良反应,使患儿在麻醉手术期间呼吸循环更平稳,家长及医护人员满意度明显提高。

Ketamine anesthesia suppressed such regions as sensory cortex, motor cortex, thalamus and callosal gyrus, which might be the key targets for ketamine action.

氯胺酮麻醉抑制感觉皮层、运动皮层、丘脑和扣带回区域信号强度,而这些区域则可能是氯胺酮作用的靶位。

Propofol pretreatment can significantly inhibit ketamine-induced HSP 70 mRNA and protein expression in the posterior cingulated cortex. It may be one of the mechanisms of inhibition of ketamine-induced psychotomimetic effect and neuronal damage by propofol.

结论异丙酚可抑制氯胺酮诱导的HSP 70 mRNA与HSP 70蛋白在大鼠后扣带回皮质区的表达,这可能是其预防或减轻氯胺酮所致精神症状和神经损害的机制之一。

Results The levels of HSP 70 mRNA and HSP 70 protein expression were significantly different among the 5 groups. Ketamine induced marked HSP 70 mRNA and HSP 70 protein expression in the posterior cingulated cortex. Propofol itself did not induce HSP 70 gene expression in this brain region. Propofol significantly inhibited ketamine-induced HSP 70 mRNA and HSP 70 protein expression in the posterior cingulate cortex in a dose-dependent manner.

结果氯胺酮可明显诱导HSP70 mRNA与HSP70蛋白在大鼠后扣带回皮质区的表达;异丙酚自身不能诱导HSP70基因的表达;预先给予异丙酚可显著抑制氯胺酮诱导的HSP70 mRNA和HSP70蛋白在这一区域的表达,且抑制效应呈剂量依赖性。

But Ketamine involves the main excitory neurotransmitter in the brain called glutamate. Ketamine functions by blocking glutamate's action on the N-methyl-D-aspartic acid receptor.

但是氯胺酮包括主要的大脑兴奋性神经递质谷氨酸,氯胺酮通过抑制谷氨酸对N-甲基-D-天冬氨酸受体起作用。

Methods Forty-five patients with hysteromyoma undergone hysteromyomectomy were randomly assigned to three groups (n=15,each group): group Ⅰ, control group without pre-emptive analgesia; group Ⅱ, the patients were administrated with 0.2 mg·kg-1 ketamine intravenously 30 min before operation; group Ⅲ, 30 mg ketamine was administrated into epidural analgesia 30 min before operation.

45例子宫肌瘤患者均于硬膜外麻醉行全子宫切除术,随机分为3组,即Ⅰ组:对照组,术前不施行超前镇痛;Ⅱ组:切皮前30 min静脉注入氯胺酮0.2 mg·kg-1;Ⅲ组:切皮前30 min将氯胺酮30 mg加入实验剂量(2%利多卡因4或5 mL)中注入硬膜外腔。3组术后均连接Graseby9300镇痛泵行患者自控硬腺外镇痛,镇痛药物为0.2%罗哌卡因加50 mg·L-1吗啡。

Results:(1) The rats produced amphetamine CPP after treated with 2 mgkg^(-1) amphetamine for 4 days. Ketamine and low, middle, high dose rhynchophylline all could eliminate the CPP effect, and the effect of rhychophylline was increased in a dose-dependent manner. Rhychophylline itself could not induce CPP in normal rats.(2) When compared with normal rats, the NR2B expression in nucleus accubens and amygdaloid of the model rats was obviously increased. Ketamine and middle, high dose rhynchophylline could decrease NR2B expression induced by amphetamine, while low dose rhynchophylline did not affect NR2B expression. Rhynchophylline had no effect on RN2B expression in normal rats.

结果:(1)建立了苯丙胺(2mgkg^(-1),连续4d)诱导的位置偏爱模型,氯胺酮及钩藤碱低、中、高剂量均可消除苯丙胺诱导的位置偏爱效应,随钩藤碱剂量增加其效应加强,且本身无精神依赖性;(2)苯丙胺模型组大鼠伏核和杏仁核NR2B蛋白表达增加,氯胺酮及钩藤碱中、高剂量抑制NR2B表达,低剂量及本身对NR2B表达无影响。

There was no effect of ketamine itself at 100 μmol/L on apoptotic cell death and [Ca2+]i. Conclusion Ketamine at 100 μmol/L can inhibit glutamate-induced apoptosis cell death in rat cultured spinal cord dorsal horn astrocytes.

结果:与C组比较,G组细胞发生了大量凋亡(P<0.01),[Ca2+]i显著升高(P<0.01);与G组比较,GK2组细胞凋亡率和[Ca2+]i明显降低(P<0.05),GK3组细胞凋亡率和[Ca2+]i显著降低(P<0.01)。

Patients with shivering grade 3–4 were allocated to receiveeither meperidine 25 mg, ketamine 0.5 mg/kg, or ketamine 0.75mg/kg IV.

寒战评分3-4级的病人分成3组,分别静脉注入哌替啶25mg 、氯胺酮0.5mg/kg 或氯胺酮0.75mg/kg 。

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