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  • KETAMINE:MEDICAL AND NON-MEDICAL USES

    作者:CHEN Char-Nie

    Ketamine is a dissociative anaesthetic.It is listed by the World Health Organisation[1] in its Model List of Essential Medicines, which are basic drugs required for any health-care system.Indeed, clinically ketamine possesses hypnotic, analgesic and amnesic effects.It is commonly used as induction and maintenance anaesthetic in surgery, especially in paediatric[2] and veterinary[3-4] surgery, with clear clinical guideline[5].In fact, it has been administered for a variety of surgical and diagnostic procedures for burn patients, aged and critically ill patients, obstetric patients, cardio-thoracic patients, outpatients and asadjunct to local and regional anaesthetics[6].

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  • 不同浓度氯胺酮对成人辅助性T淋巴细胞分化的影响

    作者:季璐璐;钱燕宁;孙杰

    Objective To investigate the effects of different concentrations of ketamine on the differentiation of human T helper (Th) cells.Methods Twenty ASA Ⅰ patients (aged 20-60 years) undergoing elective operation under general anesthesia were enrolled in this study.Peripheral venous blood samples were taken before anesthesia.Peripheral blood mononuclear cells were isolated and divided randomly into three groups (n =20 each):being incubated in the presence of 0.9% NaCl (group C),2.5 μg/ml ketamine (group K1) and 25.0 μg/ml ketamine (group K2),respectively,for 24 hours,and were then stimulated with phytohaemagglutinin for 48 hours,respectively.The percentages of Th1 and Th2 cells were detected by four-color fluorescence flow cytometry.The Th1/Th2 ratio was calculated.The levels of interleukin-2 (IL-2),IL-4,IL-6,IL-10,immunoreactive fibronectin-γ (IFN-γ) and tumor necrosis factor-alpha (TNF-α) in the supernatant were determined by cytometric bead array.Results There was no significant difference in the levels of IL-2,IL-4,IL-6,IL-10,IFN-γ and TNF-α in the supernatant,the percentages of Th1 and Th2 cells and the ratio of Th1/Th2 among groups C,K1 and K2(P> 0.05).Conclusion The sedative and anesthetic concentrations of ketamine exert no effect on the differentiation of human Th cells in vitro.

  • NMDA和GABA受体拮抗剂对帕金森模型小鼠神经细胞的影响

    作者:王传功;王旭;齐汝霞

    目的探讨Ketamine和Bicucullin对帕金森病动物模型神经细胞的影响.方法采用MPTP腹腔注射建立C57小鼠帕金森氏病模型,腹腔内分别注射Ketamine和Bicucullin,光镜下观察黑质-纹状体多巴胺神经细胞的变化.结果在Bicucullin组可见神经细胞胞膜破坏、胞核固缩、变性坏死及炎细胞浸润等;而Ketamine组可见细胞破坏减轻、炎细胞减少.Bicucullin+MPTP组与MPTP组、Ketamine+MPTP组相比,变性细胞数量明显增加(均P<0.05);而Ketamine+MPTP组与MPTP组相比,变性细胞数量明显减少(P<0.05).结论 Bicucullin可引起多巴胺神经细胞变性,可能参与了帕金森病的发生;Ketamine可引起神经细胞的修复反应,可能具有治疗作用.

  • 异丙酚对兔脊髓缺血性损伤的保护作用

    作者:董海龙;熊利泽;朱正华

    INTRODUCTION Paraplegia complicates repair of thoracoabdominal aortic aneurysms in 16% of patients[1]. This complication is caused by spinal cord ischemia secondary to aortic clamping. Many methods and drugs have been suggested to protect against ischemic spinal cord injury. However, the efficacy is controversial. Propofol, a new intravenous anesthetic, has been proved to be protective in cerebral ischemia.

  • 氯胺酮,咪唑安定,硫喷妥钠和异丙酚对大鼠皮层脑片缺血性损伤的作用

    作者:Qing-sheng XUE;Bu-wei YU;Ze-jian WANG;Hong-zhuan CHEN

    AIM: To compare the effects of ketamine, midazolam, thiopental, and propofol on brain ischemia by the model of oxygen-glucose deprivation (OGD) in rat cerebral cortical slices. METHODS: Cerebral cortical slices were incubated in 2 % 2,3,5-triphenyltetrazolium chloride (TTC) solution after OGD, the damages and effects of ketamine,midazolam, thiopental, and propofol were quantitativlye evaluated by ELISA reader of absorbance (A) at 490 nm,which indicated the red formazan extracted from slices, lactic dehydrogenase (LDH) releases in the incubated supernate were also measured. RESULTS: Progressive prolongation of OGD resulted in decreases of TTC staining.The percentage of tissue injury had a positive correlation with LDH releases, r=0.9609, P<0.01. Two hours of reincubation aggravated the decrease of TTC staining compared with those slices stained immediately after OGD (P<0.01). These four anesthetics had no effects on the TTC staining of slices. Ketamine completely inhibited the decrease of A value induced by 10 min of OGD injury. High concentrations of midazolam (10 μmol/L) and thiopental (400 μmol/L)partly attenuated this decrease. Propofol at high concentration (100 μmol/L) enhanced the decrease of A value induced by 10 min of OGD injury (P<0.01). CONCLUSION: Ketamine, high concentration of midazolam and thiopental have neuroprotective effects against OGD injury in rat cerebral cortical slices, while high concentration of propofol augments OGD injury in rat cerebral cortical slices.

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    Objective:To study the effect of ketamine combined with fluoxetine on behavior indexes and related gene expression in depression rat model.Methods:SD rats were used as experimental animals and randomly divided into control group (C group), model group (M group), ketamine group (K group), fluoxetine group (F group) and ketamine combined with fluoxetine group (KF group); chronic unpredictable stress depression models were built and different medications were given. Then behavior indicators were detected by tail suspension test and open field test; contents of monoamine neurotransmitters were determined by HPLC-electrochemical detection assay; mRNA contents of monoamine neurotransmitter-metabolizing enzymes, BDNF and its receptor were detected by PCR method.Results: (1)behavior indexes: compared with M group, behavior indexes of K group, F group and KF group were all improved; tail suspension immobility time and central grid staying time of KF group were shorter than those of K group and F group; squares crossed number, standing up number and decoration number were more than those of K group and F group; (2) molecular indexes: compared with M group, molecular markers of K group, F group and KF group were all improved; NE, 5-HT, TH, TPH, BDNF and TrkB contents in hippocampal and prefrontal cortex tissue of KF group were higher than those of K group and F group.Conclusion:Ketamine combined with fluoxetine therapy can more effectively reduce depression-related behavior; its mechanism may be related to the regulation of monoamine neurotransmitter metabolism and brain-derived neurotrophic factor expression in hippocampus and prefrontal cortex.

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