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 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.

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.

Aim To investigate the effect of thiopental sodium on the release of glutamate and GABA from synaptosomes of rats prefrontal cortex. Methods Synaptosomes were made from rats prefrontal cortex and incubated with artificial cerebral and spinal fluid (aCSF), then divided into five groups: group base release (Base), group thiopental sodium 10 ?mol?L -1 (THS 10), group thiopental sodium 30 ?mol?L -1 (THS 30), group thiopen tal sodium 100 ?mol?L -1 (THS 100) and group thiopental sodium 300 ?mol? L -1 (THS 300). Various concentrations of thiopental sodium were added to aC SF, the release of glutamate and GABA were performed under 37℃ and measured using reversed-phase high-performance liquid chromatography (RP-HPLC). When Ca 2+-independent release of glutamate and GABA were studied, Ca 2+ was omitted from aCSF.Results Compared with Base, thiopental sodium 30 , 100 and 300 ?mol?L -1 inhibited Ca 2+-dependent release of gluta mate evoked by KCl or veratridine significantly (P

0.05);in contrast, intrathecal NMDA 2.5,5,10 ng could significantly and dose dependently decrease the HPPT(P

Objective To investigate the relationship between N-methyl-D aspartate (NMDA) receptors and the hypnotic and analgesic effects of enflurane, isoflurane and sevoflurane. Methods Kunming mice weighing 18-22 g were used in this study. The experiment was carried out in 2 parts. In Part I 120 mice were randomly divided into 3 groups (n =40 each); each group received intraperitoneal (IP) enflurane 2 ml?kg-1 or isoflurane 1.2 ml?kg-1 or sevoflurane 5 ml?kg-1 . Each group was further divided randomly into 4 subgroups ( n = 10 each) and each subgroup received artificial cerebro-spinal fluid (aCSF) 10 ?l or NMDA 25, 50 or 75 ng in 10 ?l aCSF injected into the lateral ventricle of the brain as soon as the animals lost righting reflex. The time for the recovery of righting reflex was recorded. In Part Ⅱ 160 mice were randomly divided into 4 groups ( n = 40 each) : ( 1) control group received no inhalation anesthetic; (2) enflurane group received enflurane 1.5 ml?kg-1 subcutaneously s.c. ; (3) isoflurane group isoflurane 0.8 ml?kg-1 s.c. and (4) sevoflurane group sevoflurane 4.5 ml ?kg-1 s.c. Each group was further divided randomly into 4 subgroups ( n = 10 each). Each subgroup received intrathecal (IT) aCSF 10 ?l or NMDA 2.5 ng or 5.0 ng or 10 ng in aCSF 10 ?l at 10 min after subcutaneous injection of inhalation anesthetic. 6% acetic acid 0.1 ml?10 g-1 was injected IP at 1 min after intrathecal administration. The number of writhing induced by acetic acid was recorded. Results In Part Ⅰ of the experiment there was no significant difference in the duration of anesthesia induced by the 3 inhalation anesthetics between the 4 subgroups. In Part Ⅱ subcutaneous injection of the 3 inhalation anesthetics significantly reduced the number of writhing induced by IP acetic acid. In control group which received no inhalation anesthetic there was no significant difference in the number of writhing between the 4 subgroups. In the 3 inhalation anesthetic groups NMDA5. 0 and 10 ng IT significantly increased the number of writhing induced by IP acetic acid in a dose dependent manner as compared with aCSF subgroup. Conclusion Cerebral NMDA receptors do not play an important role in the hypnotic effect of enflurane, isoflurane and sevoflurane while spinal NMDA receptors are involved in the analgesic effect of the 3 inhalation anesthetics.

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.