Objective To investigate the inhibitory effects of fentanyl on GABAA receptors in hippocampal pyramidal neurons of rat.Methods Pyramidal neurons were acutely isolated from 3-10 day old SD rats of either sex by enzymatic-mechanic method. GABAA receptor mediated currents ( IGABA) were recorded using voltage clamped whole cell patch clamp technique in gap-free mode at the holding potential (VH) of - 50 mV. Current-voltage relationship of IGABA was obtained in ramp protocol ranging from + 30 mV to - 110 mV and lasting for 1 600 ms. Data were collected by using a system consisting of Axopatch 200B patch-clamp amplifier, Pentium Ⅲ computer and Digidata 1200 interface. All experiments were performed at room temperature (22-25℃). Five to twelve neurons were used for each fentanyl concentration. The effects of fentanyl from 1.0 ? 10-5 ?mol?L-1 to 10. 0 ?mol?L-1 were evaluated by the inhibition rate of the peak amplitude of IGABA, the desensitization time constant (?des) of IGABA and the reversal potential (Ecl- ) of IGABA. A ?-opioid receptor selective antagonist CTAP 1 ?mol?L-1 was applied and its effects on fentanyl were recorded. Results (1) GAB A 1-1 000 ?mol?L-1 induced inward currents (IGABA) dose-dependently with an EC50 of 23.73 ?mol?L-1.IGABA induced by GABA 30 ?mol?L-1 was blocked by bicuculline 1 ?mol?L-1. (2) Fentanyl depressed IGABA dose-dependently with EC50 of 0.011 ?mol?L-1 and shortened the rdes of IGABA.(3) The inhibitory effects of fentanyl on IGABA were antagonized by CTAP. (4) Fentanyl 0.01 ?mol?L-1 and CTAP did not influence the reversal potential of IGABA (Ecl- -3.0 mV) .Conclusion Fentanyl inhibits the function of GABAA receptors through ?-opioid receptors in hippocampal pyramidal neurons. Hippocampus may play a role in the neuroexcitatory effects of opioids.

Objective To evaluate the effect of intrathecal IL-10 gene on neuropathic pain induced by chronic constriction injury (CCI) to the sciatic nerve. Methods Sixty female SD rats weighing 230-250 g were anesthetized with pentobarfaital. Right sciatic nerve was exposed at the midthigh level and 4 ligatures were placed on the sciatic nerve with 4.0 catgut at 1mm interval. Intrathecal catheter (PE-10 tubing) were inserted at L5,6 interspace and correct placement was confirmed by outflow of CSF. The animals were randomized into 5 groups ( n = 12): group Ⅰ sham operation; group Ⅱ CCI; group Ⅲ,Ⅳ and Ⅴ received intrathecal (IT) normal saline (NS) (Ⅲ) or pcDNA 3.1 (Ⅳ) or pcDNA 3.1-IL-10 (Ⅴ) 3 days after CCI when the animals developed thermal hyperalgesia. Threshold to noxious thermal stimuli was measured before CCI (baseline), before and 2, 4, 7, 10 and 14 days after IT injection. CSF was collected on 1, 3, 7 and 10 days after IT injection for determination of CSF IL-10 concentration. Six animals were killed on 3rd and 14th days after IT injection respectively in each group and the sciatic nerve, lumbar segment of spinal cord ( L3-6) and hippocampus were isolated and blood was collected for determination of IL-10 mRNA expression (by RT-PCR) (on 3rd day after IT) and TNF-? content (on 14th day after IT) .Results Paw removal latencies were significantly longer 2-14 days after IT injection in group Ⅴ(CCI + pcDNA 3.1-IL-10) than in group Ⅲ (CCI + NS) and Ⅳ (CCI + pcDNA 3.1). The IL-10 mRNA expression in sciatic nerve, lumbar segment of spinal cord and hippocampus was significantly higher 3 days after IT injection while their TNF-? contents were significantly lower 14 days after IT injection in group Ⅴ than in the other 4 groups. The CNS IL-10 concentration on day 1-7 after IT injection was significantly higher in group Ⅴ than in the other 4 groups. Conclusion Intrathecal IL-10 gene injection can ease pain induced by CCI of the sciatic nerve through inhibition of inflammatory response.

Objective To evaluate the feasibility of using auditory evoked potential index(AAI) to monitor the depth of nitrous oxide anesthesia. Methods Sixteen ASAⅠ-Ⅱpatients aged 23-64 years, weighing 51-86 kg scheduled for elective surgery under general anesthesia were studied. Patients with psychoneural diseases and hearing disturbances were excluded. The patients were premedicated with phenobarbital sodium 0.1g and atropine 0.5mg. AAI, BIS, 95% SEF, BP, HR, SpO2 monitoring were started before induction of anesthesia. The patients were preoxygenated for 5 min using a close-fitting face mask and 100% O2 at l0L?min-1 . Inhalation of nitrous oxide was then started. Nitrous oxide concentration was gradually increased in increments of 10% from 0% to 70% . AAI, BIS and 95%SEF were recorded and observer's assessment of alertness/sedation (OAA/S) scores were measured at each 10% increment of end-tidal nitrous oxide concentration which was maintained for 5 min. The correlation between AAI, BIS, 95% SEF and OAA/S scores was analyzed. Results OAA/S scores and AAI decreased as the nitrous oxide concentration increased. AAI correlated closely with OAA/S scores and end-tidal nitrous oxide concentration (the coefficients of Spearman' s rank correlation ? = - 0.739, 0.837, P

Objective Potassium channel is essential for excitability of neurons and is involved in the regulation of information transmission. The purpose of this study was to investigate the effect of propofol on the voltage-gated potassium channels in rat hippocampal pyramidal neurons. Methods SD rats of 5-15 days old were decapitated and brain was immediately removed. Hippocampal pyramidal neurons were freshly isolated. Whole-cell patch clamp recordings were made. Voltage-dependent sodium and calcium currents were inhibited by TTX 1?mol?L-1 and CdCl2 400 ?mol?L-1 added to the perfusate. The effects of propofol on transient outward potassium currents and delayed rectifier potassium currents were studied and also the kinetics of channels. Results All the channels studied were reversibly inhibited by propofol in a dose-dependent manner. EC50 of propofol on transient outward potassium channels and delayed rectifier potassium channels were (71?18) ?mol?L-1 and (37?18) ?mol?L-1 respectively. The maximum inhibition rates were 52%?3% and 32%?5% .Conclusion Propofol reversibly inhibits potassium currents in a does-dependent manner. It is inferred that propofol affects the excitability of hippocampal neurons.

Objective To investigate and compare the actions of vecuronium and atracurium on adult and embryonic-type nicotinic acetylcholine receptors (?-and ?-nAChR) at skeletal muscle cell membrane. Methods The adult and embryonic nAChRs were heterologously expressed in HEK 293 cells. Peak currents induced by actions of vecuronium and atracurium at ?-and ?-nAChR were recorded in HEK 293 cells, using whole cell patch clamp technique. Results Vecuronium and atracurium competitively inhibited ?-and ?-nAChR in HEK 293 cells. The inhibitor concentrations for half-maximal response (IC50) for vecuronium and atracurium ate-nAChR were (8.3 ? 2.6) ?mol/L and (24.2 ? 10.5) ?mol/L respectively; The IC50 values for vecuronium and atracurium at e-nAChR were (55.0 44 28.4) ?mol/L and (183.2 ? 39.2) ?mol/L respectively.Conclusion According to IC50 values for both adult and embryonic type nAChR, vecuronium is more potent than atracurium on e-and 7-nAChR. Embryonic nAChR is less sensitive to vecuronium and atracurium than adult-type nAChR.

Objective To evaluate the effects of propofol and thiopontal on calcium and potassium channels in rat ventricular myocytes and to elucidate the underlying mechanisms of their inhibitory effect on myocardium. Methods Freshly isolated ventricular myocytes were prepared from hearts of rats by trypsin. The effects of propofol and thiopental on L-type calcium current(Ica) and delayed rectifier potassium current(IK)were compared using whole-cell patch clump technique. Results Propofol and thiopontal produced a concentration-dependent inhibition of Ica. Peak concentration of propofol(50 ?mol?L~(-1)) and thiopental(100 ?mol?L~(-1)) during induction of anesthesia decreased Ica by 28% and 46% and shifted the steady-state inactivation curve to more negative voltage, but had no effect on the steady-state activation curve. Propofol and thiopental also decreased IK in a concentration-dependent manner, but the effects of both anesthetics on IK were smaller compared with their effects on Ica. Conclusion The findings of this study suggest that the negative inotropic of propofol and thiopental are, at least in part, related to decrease in Ca~(2+) trans-sarcolemmal current by accelerating L-type calcium channel inactivation. Both anesthetics decrease delayed rectifier potassium current, thus partially antagonizing the effect of decreased calcium current.

Objective To investigate the effects of pancuronium on nicotinic acetylcholine receptors (nAChRs) in pheochromocytoma cells (PC12 cells) and to determine if pancuronium has direct effects on PC cells.Methods PC12 cells (purchased from Institute of Cytology, Chinese Academy of Science) were cultured in DMEM containing penicillin and glutamine. nAChR in PC12 cells were stimulated with different concentrations of Ach ( 10, 30, 100, 300, 1 000 ?mol?L-1 ). Ach-mediated inward currents were recorded using whole-cell patch clamp technique with holding potential set at - 80 mV. To investigate the effects of pancuronium on nAChR in PC cells, the PC12 cells were perfused with different concentrations of pancuronium (0.01,0.1, 1, 10, 100, 1 000 ?mol ? L-1 ) before Ach 1 ?mol?L-1 was added. Results Inward currents were elicited by stimulation of nAChR with Ach in a concentration-dependent manner. 93.7% of nAChRs could be activated by 1 ?mol ? L1 Ach. Pancuronium reversibly suppressed the currents in a concentration-dependent manner compared to the control currents elicited by 1 ?mol?L-1 Ach. 1 ?mol?L-1 pancuronium could almost completely suppressed the currents elicited by 1 ?mol ? L-1 Ach.Conclusion Pancuronium could inhibit nAChR in PC12 cells and reduce catecholamine release.

The neuromuscular and cardiovascular effects and endotracheal intubating conditions of bolus intravenous rocuronium 0.6mg/kg or 0.75mg/kg in 20 patients under balanced anesthesia,were studied, Intubating conditions were evaluated as excellent or good in all patients,except for one with poor intubating conditions following 0.6mg/kg. Onset times of both groups were 73.1 s and 67.1 s;neuromuscular blockade durations 24.9min and 32.0min; 25% recovery times 37.3min and 45.4min; 75% recovery times 46.4min and 58.7min;recovery index 9.1min and 13.3min,respectively. The cardiovascular effects after rocuronium in both groups were minimal.

Objective: To analyse correlation of bispectral index,spectral edge frequency of electroencephalogram with midazolam-induced sedation. Method: 30ASA grade Ⅰ-Ⅱ adult patients, undergoing elective surgery under regional anesthesia were randomly devided into three groups according to intravenous bolus doses of midazolam,i, e. group Ⅰ:0.05mg?kg~(-1),group Ⅱ:0.1mg?kg~(-1),group Ⅲ:0.2mg?kg~(-1). After an intravenous bolus dose of mida zolam was administered,both bispectral index (BIS), 95% spectral edge freguency (SEF) of electroencephalogram were monitored and their correlation with midazolam induced sedation was analysed. Result: Both BIS and 95% SEF-correlated with midazolam-induced sedation significantly (r= 0.86,0.73, P

Objective: To examine the effects of midazolam-induced sedation on heart rate variability (HRV). Method:Fifteen ASA Ⅰ- Ⅱ adult patients,undergoing elective surgery under lumbar epidural anesthesia were randomly selected. An intravenous bolus dose of midazolam(1.5mg) was administered every 3-5 minutes until patients' sedation levels assessed by observers assessment of alertness sedation(OAA/S) scale had scores of 1. Spectral analysis of HRV was performed at different OAA/S scores and at 3min,5min and 10min following OAA/S score of 1. Result:All frequency components of HRV were significantly reduced as patients' OAA/S scores decreased,especially low frequency (LF) and total power. Midazolam decreased normalized unit power of LF from 33.5%?8.9% to 16.65?9.6% and increased normalized unit power of high frequency(HF) from 11.7%?4.2% to 20.5%?26.5%. LF/HF ratio also reduced. Conclusion:Midazolam shiftes the balance of autonomic nervous activity toward the parasympathotonic.