Evaluation of high-concentration sevoflurane for induction and nasotracheal intubation without muscle relaxant for infants with different pulmonary blood flow undergoing surgery for congenital heart diseases / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Inhalational anesthesia with sevoflurane for endotracheal intubation without muscle relaxant is now used widely for pediatric patients. This study assessed the efficacy and safety of induction with high concentration sevoflurane and of nasotracheal intubation without muscle relaxant in infants with increased or decreased pulmonary blood flow (PBF) and undergoing surgery for congenital heart diseases.</p><p><b>METHODS</b>Fifty-five infants aged 2 - 12 months, weighing 4.7 - 10.0 kg, and scheduled for congenital cardiac surgery were enrolled. Subjects were divided into those with increased (IPBF group, n = 29) and decreased (DPBF group, n = 26) pulmonary blood flow. All infants received inhalational induction with 8% sevoflurane in 100.0% oxygen at a gas flow rate of 6 L/min. Nasotracheal intubation was performed 4 minutes after induction. Sevoflurane vaporization was decreased to 4.0% for placement of a peripheral intravenous line and invasive hemodynamic monitors. Five minutes later, sedatives and muscle relaxant were administered and the vaporizer was adjusted to 2% for maintenance of anesthesia. Bispectral index (BIS) scores, circulatory parameters, satisfactory and successful intubation ratios, adverse reactions, and complications of intubation were recorded.</p><p><b>RESULTS</b>Times to loss of lash and pain reflexes were longer for the DPBF group (P < 0.01). Satisfactory intubation ratios were 93.1% and 61.5% for the IPBF and DPBF groups, respectively (P = 0.008). Successful intubation ratios were 96.6% and 76.9% for the IPBF and DPBF groups, respectively (P = 0.044). Following sevoflurane inhalation, blood pressures decreased significantly in the IPBF group but remained stable in the DPBF group. BIS scores declined to similar stable values, and a "nadir BIS" was recorded for both groups. No obvious adverse reactions or complications of intubation were noted perioperatively.</p><p><b>CONCLUSIONS</b>Induction with high concentration sevoflurane, although faster for infants with IPBF, is safe for infants with IPBF or DPBF. However, nasotracheal intubation without muscle relaxant after induction with high concentration sevoflurane is less successful and less satisfactory for infants with DPBF and should be used with caution in this patient group.</p>

Effects of naloxone on the expression of stem cell factor and C-kit receptor in combined oxygen-glucose deprivation of primary cultured human embryonic neuron in vitro / 中国医学科学院学报

<p><b>OBJECTIVE</b>To explore the effects of naloxone on the expression of c-kit receptor (c-kit R) and its ligand stem cell factor (SCF) in human embryo neuronal hypoxic injury.</p><p><b>METHODS</b>Serum-free cerebral cortical cultures prepared from embryonic human brains were deprived of both oxygen and glucose which would set up an environment more likely with that of in vivo ischemic injury. Neurons in 24-well culture plates were randomly divided into four groups: control group, hypoxia group, naloxone 0.5 microg/ml group and naloxone 10 microg/ml group. MTT assay and biological analysis were performed to study the cell death and the changes of extracellular concentrations of lactate dehydrogenase (LDH) after combined oxygen-glucose deprivation. Neurons in 25 ml culture flasks were also randomly allocated into four groups as previously described. Intracellular total RNA were extracted at different time points: pre-hypoxia, immediately after hypoxia, and 3, 6, 12, and 24 hours after reoxygenation. The changes of SCF/c-kit R mRNA expression in hypoxic neurons treated with different concentrations of naloxone pre and post oxygen-glucose deprivation were determined with RT-PCR.</p><p><b>RESULTS</b>The cell vitality detected by MTT assay decreased significantly in hypoxia group and naloxone 0.5 microg/ml group when compared with control group (P<0.01), while no significant difference was found between naloxone 0.5 microg/ml group and hypoxia group or between naloxone 10 microg/ml group and control group. Extracellular concentration of LDH significantly increased in hypoxia group (P<0.05), while no difference was found between naloxone 0.5 microg/ml group and control group, between naloxone 0.5 microg/ml and hypoxia group, or between naloxone 10 microg/ml and control group (all P>0.05). Immediately after oxygen-glucose deprivation, the expression of SCF/c-kit R mRNA increased significantly (P<0.01). Among those the expression of SCF presented a distribution of double-peak value within 24 hours. After treated with different concentrations of naloxone, the peak value of each group were delayed to appear and went down with the increasing of naloxone concentration. The peak values in all treated groups were significantly different from that in control group (P<0.01).</p><p><b>CONCLUSIONS</b>The expression of SCF/c-kit R mRNA increases at the early stage after combined oxygen-glucose deprivation. Naloxone 0.5 microg/ml can attenuate cell injuries and regulate the expression of SCF/c-kit R. Naloxone may protect neurons by modulating the expressions of some cytokines.</p>

Effects of naloxone on glutamate release in combined oxygen-glucose deprivation of primary cultured human embryo neuron / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the effects of naloxone on glutamate release in combined oxygen-glucose deprivation of primary cultured human embryo neurons.</p><p><b>METHODS</b>The primary cultured embryonic human cortical neurons were demonstrated by immunocytochemical stain of neural filament (NF). The neurons were randomly allocated into control group, hypoxic group, and experimental group. The experimental group was further divided into three subgroups pretreated with different concentrations of naloxone (0.25, 5, 10 microg/ml). The neurons of hypoxic group and experimental group were deprived both oxygen and glucose for 1 hours followed by 24 hours of reoxygenation. Meanwhile, we used 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, high performance liquid chromatography (HPLC), and biological analysis to study the survival rate of neurons and the changes of extracellular glutamate and lactate dehydrogenase (LDH) levels after 24 hours of reoxygenation.</p><p><b>RESULTS</b>One hour of oxygen-glucose deprivation followed by 24 hours of reoxygenation was associated with a large increase in extracellular LDH and glutamate and a significant decrease of cell vitality (P < 0.01). Naloxone exerted a concentration-dependent protection against neuronal injury provoked by combined oxygen-glucose deprivation. After reoxygenation, the extracellular concentrations of glutamate gradually decreased (P < 0.05, P < 0.01, respectively) and cell vitality increased (P < 0.01) with increase of the concentration of naloxone compared with control group. All of them returned to control level when naloxone was up to 10 microg/ml (P > 0.05).</p><p><b>CONCLUSION</b>Naloxone protects neurons from hypoxic injury by inhibiting the release of glutamate and therefore alleviating the exciting toxicity.</p>

Effects of ketamine on anoxia-reoxygenation induced glutamate release from cerebral cortex neurons of fetal rats / 中华麻醉学杂志

Objective To investigate the effects of ketamine on anoxia-reoxygenation(A/R)induced glutamate release from cerebral cortex neurons.Methods Primary cultured neurons obtained from cerebral cortex of fetal Wistar rats(16-18 d)were randomly divided into 3 groups:Ⅰcontrol group;ⅡA/R group andⅢketamine pretreatment+I/R group.The control group was not subjected to A/R while A/R group was exposed to anoxic air(95% N_2+5% CO_2)for 5 h followed by 24 h reoxygenation.In groupⅢdifferent doses of ketamine were added to the culture media before anoxia and the final ketamine concentrations were 1,20 and 100?mol?L~(-1) respectively.The extracellular glutamate concentration was detected at the end of 24 h reoxygenation.Results The extracellular glutamate concentration was significantly higher after 24 h reoxygenation in A/R group than in control group.Ketamine 20 and 100?mol?L~(-1) significantly inhibited glutamate release from the neurons induced by A/R in a dose-dependent manner.Conclusion Ketamine can inhibit glutamate release from neurons induced by A/R in a dose-dependent manner.