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 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.

AIM: To study the effects of droperidol on the enhancement of persistent sodium currents induced by in vitro ischemia-like condition in isolated rat CA1 paramidal neurons. METHODS: Whole-cell patch-clamp recordings were made from enzymatically isolated rat CA1 hippocampal paramidal neurons. Ischemia was induced by oxygen and glucose deprivation. RESULTS: All of 3, 10 ,and 30 ?mol?L -1 of droperidol significantly inhibited the enhancement of persistent sodium currents induced by ischemia, but the different concentrations did not show significant difference. CONCLUSION: Droperidol in clinical concentration can inhibit the enhancement of persistent sodium current induced by ischemia.

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.

Objective: To explore the effects of desflurane on systemic and hepatic hemodynamics and oxygen delivery to the liver. Method: 11 healthy mongrel dogs were anesthetized with 0.5 and 1.0 MAC desflurane respectively. The changes of systemic, pulmonary and hepatic hemodynamics,systemic oxgen delivery and consumption,oxygen delivery to the liver were measured continuously. Blood flow of hepatic artery and portal vein was monitored with electromagnetic flowmeter. Result: During inhalation of 0.5 MAC desflurane,HR.MAP.SVR,portal vein and total hepatic oxygen delivery decreased significantly(P

Objective The effect of lidocaine and bupivacaine on the Na+ current of dorsal horn neurons was observed to further evaluate the mechanism of local anesthetics . Methods The dorsal horn neurons of the SD neonates(0-7 d) were isolated acutely. Under the condition of holding voltage -80mV , and testing voltage -30mV with duration of 20 ms , the whole-cell patch-clamp technique was applied to recording the changes of voltage-gated Na+ currents following the administration of lidocaine or bupivacaine at 50-1000?mol/L.Results The voltage-gated Na+ currents ranged from 0.5-8nA peak amplitude , was inhibited by lidocaine and bupivacaine at clinical concentrations, the inhibitory degree was parallelly correlated with the concentration of local anesthetics(r=0.949 and 0.847 ,P

Objective To study the effects of propofol on the whole-cell sodium currents in rat sympathetic neurons in order to investigate the mechanisms of propofol-mediated peripheral vasodilation.Methods Whole-cell patch-clamp recordings were made from enzymatically isolated rat superior cervical sympathetic neurons.Results Propofol dose-dependently blocked the whole-cell sodium currents evoked by a voltage step from a holding potential of -- 80mV to 0mV with a mean IC50 value of 32. 19?mol/L (r = 0. 982, P

Objective To study the effects of desflurane on Ca 2+-ATPase activity isolated rat cardiac myocyte plasma membrane ,for the mechanisms of its inhibitory myocardial function.Methods The effects of different concentration desflurane(0%-11%) on Ca 2+-ATPase activity were studied at different calcium concentration(04-20?mol/L) and at 25℃ or 37℃Results Ca 2+-ATPase activity wan depressed by desflurane,the greater inhibitory effect,the higher desflurane concentration,and more severely at low calcium concentration or at 37℃ than at high calcium concentration or at 25℃Conclusions At clinical concentration desflurane produces tha inhibitory effect on rat cardiac myocyte plasma membrane Ca 2+-ATPase activity dose-dependently,which may in part explain its depression on myocardial function.