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.

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 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.

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.