Objective To compare the impacts of four different intravenous anesthetic agents on middle cerebral artery blood flow velocity(V‐MCA) during the anesthesia induction period .Methods Totally 80 cases were randomly divided into four groups (n=20) ,maintenance drugs of anesthesia were propofol 2 .00 mg/kg ,etomidate 0 .30 mg/kg ,midazolam 0 .15 mg/kg and dezocine 0 .20 mg/kg respectively ,the bispectral index (BIS) value was dropping to below 50 ,the endotracheal intubation and mechanical ventilation were performed .The transcranial Doppler (TCD) monitoring was adopted to monitor and record middle cerebral artery mean flow velocity (Vm‐MCA) ,mean arterial pressure (MAP) ,heart rate (HR) ,systolic blood pressure (SBP) ,diastolic blood pressure (DBP) in the four groups before induction after entering operation room (T0 ) ,at1 min before intubation (T1 ) ,immediate intubation (T2 ) ,at 1 min after intubation (T3 ) ,3 min after intubation (T4 ) ,5 min after intubation (T5 ) .Results Except for the midazolam group ,Vm‐MCA at T1 in the other three groups were significantly lower that that in the T0 group (P< 0 .05);Vm‐MCA ,SBP ,DBP after intubation in the midazolam group and the etomidate group were significantly increased compared with the basic values ,while the difference between the propofol group and the dezocine group had no statistical significance (P>0 .05) .Con‐clusion midazolam and etomidate are weaker than propofol and dezocine in the aspect of inhibiting the middle cerebral arterial blood flow fluctuations caused by intubation .

Aim To investigate the effects of propofol and lidocaine on P2X7-gated currents and the interaction of both drugs.Methods RAW2647 macrophages were cultured,whole-cell patch clamp technique was used to record the P2X7-gated currents induced by ATP with two times EC50 level under 1~100 ?mol?L-1 propofol or 10~1 000 ?mol?L-1 lidocaine. Then,propofol of IC50 level and lidocaine with 10~1 000 ?mol?L-1 were administered,and the P2X7-gated currents were recorded.Results Propofol and lidocaine could inhibit P2X7-gated currents in a concentration-dependent manner,and the IC50 level was (36.5?5.3) ?mol?L-1 and (223?34) ?mol?L-1,respectively. Lidocaine with high concentration (300 ?mol?L-1,1 000 ?mol?L-1) following the administration of propofol of EC50 level could increase the P2X7-gated currents(P

Objective To investigate the role of neurokinin-1 receptor (NK-1R) in the anti-nociceptive effect of enflurane, isoflurane and sevoflurane in mice. Methods Three hundred and twenty Kunming mice of both sexes weighing 20-25 g were randomly divided into4 groups (n =80 each): group normal saline (group NS);group enflurane (group E); group isoflurane (group I) and group sevoflurane (group S). Normal saline (NS) 1.0ml/kg, erflurane 0.5 ml/kg, isoflurane 0.4 ml/kg and sevoflurane 2.0 ml/kg were injected intraperitoneally in NS,E,I and S groups respectively. Each group was further divided into 4 subgroups receiving intrathecal NS 5 μl and Sar-SP (NK-IR agonist) 20, 40 and 80 ng respectively at 5 min after intraperitoneal injection of inhalation anesthetics. The anti-nociceptive effect of the inhalation anesthetics was assessed by tail flick latency (TFL) (the latency for removal of the tail from the path of heat source) and paw-licking time (PLT) after intraplantar formalin injection. Results lntraperitoneal enflurane, isoflurane and sevoflurane significantly prolonged TFL and shortened PLT. Intrathecal Sar-SP 20, 40 and 80 ng significantly shortened TFL dose-dependently but had no significant effeet on PLT as compared with control subgroup. Conclusion NK-1R is involved in the anti-nociceptive effect of enflurane, isoflurane and sevofluran on thermal pain but not chemical and inflammatory pain.

Objective To investigate the effects of propofol on P2X7 receptor activition and IL-1β production induced by endotoxin in murine RAW264.7 macrophages. Methods RAW264.7 macruphages were treated with LPS (1 μg/ml) for 4 h to induce the production and release of IL-1β, and pretreated with BBG (specific P2X7 receptor antagonist) 1 μmol/L or propofol 1-100 μmol/L for 20 min before LPS stimulation, and IL-1β release was measured using ELISA kit. Whole-cell patch clamp technique was used to record the P2X7-gated currents induced by 1 mmol/L ATP, the cells were exposed to propofol with 1-1 000 -μmol/L for 4 min, and the IC_(50) level of propofol was achieved. Western blot technique was used to measure the production of pro-lL-1β protein and IL-1β protein intracellularly after LPS treatment for 4 h under different concentrations of propofol. Results IL-1β was released from RAW264.7 macrophages after LPS stimulation, which was decreased by propofol, and the IC_(50) level of propefol was (24±3) μmol/L. P2XT-gated currents were inhibited by propofol, and the IC_(50) level was (33±5) μmol/L. Pro-IL-1β protein intracellularly was up-regulated after LPS stimulation, and propofol with 3-100 μmol/L decreased the up-regulation of pro-IL-1β intracellularly induced by LPS. Conclusion Propefol could inhibit IL-1β release from RAW264.7 macrophages treated by LPS, which is mediated by inhibiting P2X7 receptor activition and decreasing the production of pro-IL-1β intracellularly.

AIM: To investigate the dynamic changes of ATPases and NOS activities and NO production at different anesthesia phases using thiopental and propofol andifferent anesthetic phases (induction, anesthesia, restoration, and awake), the activities of NOS and ATPase and NO production in cortex and brain stem were meagroup. RESULTS: Ca2+ -ATPase and Na+ ,K+ -ATPase activities in the cortex and brain stem were significantly decreased after administration ofthiopental and propofol,especially at induction, anesthesia, or even restoration phase of thiopental group (P＜0.05, P＜0.01) and at anesthesia phase of propofol group (P＜0.05). NOS activities and NO production decreased from induction to restoration phase with thiopental and propofol anesthesia (P＜0.01). The parameters were returned near to the normal at awaken phase. CONCLUSION: Activities of ATPases and NOS and the production of NO may mediate the anesthesia effects of thiopental and propofol in the rat cortex and brain stem.

Objective To investigate the effect of thiopental sodium (TPS) on spontaneous and KCl-evoked glutamate release from prefrontal cortical synaptosomes in rats and the effect of bicuculline on this effect ofTPS.Methods SD rats of both sexes (200-250 g) were decapitated and brains were removed. The prefrontalcortex was dissected and added to ice-cold sucrose solution and homogenized. The homogenate was centrifuged at1000 g at 0℃-4℃ for 5 min. The supernatant was again centrifuged at 12 000 g for 20 min. The sediment wascrude synaptosomes, which was added to artificial cerebro-spinal fluid (ACSF). The crude synaptosomes weredivided into 5 groups (n = 8): control group and 4 TPS groups. In control group no TPS was added while in TPSgroups different concentrations of TPS was added and the final concentration of TPS was 10, 30, 100, 300?mol?L~(-1) respectively. The synaptosomes were then placed with or without KCl in water bath at 37℃ for 15 min. Thespontaneous or KCl-evoked glutamate release was measured using high-performance liquid chromatograph (HPLC).In another set of experiment bicuculline 0. 1 mmol?L~(-1) was added to ACSF in each group before 15 min water bathto see if it could antogonize the effect of TPS on glutamate release. Results TPS 30, 100 and 300 ?mol?L~(-1)could significantly inhibit the spontaneous or KCl-evoked glutamate release compared with control group (P0.05). Bicuculline 0. 1 mmol?L~(-1) had no effect on the glutamate release in control group but could antagonize the inhibitory effect of TPS on glutamate release. Afteraddition of bicucculline the glutamate released in control group was not significantly different from that in the TPSgroups.Conclusion TPS sodium can inhibit the spontaneous or KCl-evoked glutamate release from prefrontalcortical synaptosomes in a concentration-dependent manner. The inhibitory effect is mediated by GABA_A receptors.

The analgesic, sedative and convulsive effects of procaine were determined by animal experiments. The analgesic ED50 of procain were 21.7mg/kg or 52.8ug/ each (iv or icv, hot plate) and 29.2mg/kg or 52.2ug/ each (iv or icv,electral stimulation) in mice.Procaine In subthreshold dose had additive hypnotic effect of phenobarbital in mice and rabbits, but could not de crease spontaneous activity in mice.The convulsive ED50 of procaine were 13.5mg/kg (iv) or 2.4mg/each (icv) in rabbits.There was no influence on the righting reflex in all the experiment animals when iv or icv procaine was given alone.These results suggest that the analgesic and sedative effects of procaine are weak, but may be potentiated when administered concomitantly With other potent drugs.

The interaction between sodium oxybate and ketamine were studied in conscious animals. Sodium oxybate increased the LD_(50) of ketamine, increased the incidence of sleep caused by ke tamine and prolonged the sleep duration and potentiated analgesic action of ketamine. Sodium Oxybate didn't effect the respiratory and circulatory function in rabbits. The results showed sodium oxybate po tentiated the anesthetic action of ketamine and reduced the side effect of ketamine. So It is suggested that sodium oxybate has the anesthetic synergism with ketamine in animals.

Objective To investigate the effect of propofol on the whole-cell sodium currents in rat hippocampal pyramidal neurons in order to determine whether brain sodium channels are involved in the molecular mechanism of action of propofol. Methods The pyramidal neurons were enzymatically isolated from rat hippocampus. The experiment was divided into seven groups: in group 1-4 (propofol groups) different amount of propofol (dissolved in intralipid) was added to bath solution and four solutions of different propofol concentration-10, 30, 50 and 100 ?mol?L-1 were prepared (Pro10 , Pro30 , Pro50 and Pro100 ); in group 5-6 intralipid alone (without propofol) was added to bath solution and two solutions of intralipid concentration equal to that of Pro50 and Pro100 were prepared; in group 7 neither propofol nor intralipid was added to the bath solution. The effect of propofol and intralipid on the whole-cell sodium channel currents were assessed using patch-clamp technique.Results When the holding potential was - 100 mV, the four concentrations of propofol (10, 30, 50 and 100 ?mol?L-1) reduced peak sodium currents by 14.4%?8.7% , 42.9%?8.8% , 67.2?18.1% and 85.1%?14.9% respectively, with a mean LC50 of 32.5 ?mol?L-1.The two concentrations of intralipid did not significantly affect the peak sodium currents. Conclusion Propofol significantly inhibits the brain sodium channel currents in a dose-dependent manner, indicating a possible role of brain sodium channel suppression in propofol anesthesia.

Objective To determine the effect of enflurance on nitric oxide synthase (NOS) activity and nitric oxide (NO) content in different brain regions at different anesthesia stages.Methods Forty female SD rats weighing 250-350 g were randomly divided into five groups of 8 animals each, group 1: control; group 2: induction of anesthesia; group 3: maintenance of anesthesia; group 4: recovery from anesthesia and group 5: complete recovery. Animals were placed in a special glass anesthesia box. The concentration of enflurane in the box was measured by anesthesia gas monitor (Normac). The induction of anesthesia started from staggering of the animal to loss of righting reflex, maintenance of anesthesia from 1 min after loss of righting reflex, recovery of anesthesia from recovery of righting reflex to staggering after enflurance anesthesia was discontinued and glass box was opend and complete recovery from 1h after recovery of righting reflex. The animals were decapitated at different stages of anesthesia. Cerebral cortex, hippocampus and brain stem were immediately removed on ice and frozen in liquid nitrogen. Their NOS activity and NO content were measured by spectroscopic analysis. Results The average duration from the beginning of 2.2% enflurane inhalation to loss of righting reflex was (169?30) s. The average duration of anesthesia induction was (138?36)s. The maintenance of anesthesia lasted (229?30) s and the recovery period averaged (266?41) s. The NOS activity and NO content in different brain regions began to decrease during induction of anesthesia and reached their lowest level during maintenance of anesthesia, began to increase during recovery from anesthesia and returned to preanesthetic level during complete recovery. Conclusion Enflurane significantly inhibits the NOS activity and NO content in the brain. The inhibits is closely related to the depth of anesthesia. NO is a message transmitter in central nervous system and may be involved in the mechanism of enflurane anesthesia.