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

AIM To investigate the effects of propofol on Na +, K + ATPase and Ca 2+ ATPase activities in rat brain. METHODS Forty rats were divided randomly into five groups. The animals were administered intraperitoneally (ip) propofol 100 mg?kg -1 or equal volume of normal saline (control group) respectively. These rats were immediately decapitated before (induction group) and after (anesthesia group) the disappearance of righting reflex, and when righting reflex appeared again (recovery group), and rats were completely conscious (awake group). Brain tissues were dissected on ice, then homogenized and centrifuged. Na +, K + ATPase and Ca 2+ ATPase activities were estimated by spectrophotometry. RESULTS Propofol 100 mg?kg -1 ip significantly inhibited Na +, K + ATPase and Ca 2+ ATPase activities of cortex, hippocampus and brain stem as compared with that of normal saline group ( P

Aim To investigate the relationship between spinal cord noradrenergic neurons ? 1 adrenoceptors and the spinal analgesia of ketamine. Methods Kunming mice were used. Analgesia tests were investigated with warm water tail flick test. The effects of intrathecal injection (ith) of ketamine (50,100,200 ?g)on tail flick latency of animals were observed. And the effect of pretreatment with intrathecal 6 hydrodoapa(6 OHDA, 6?g ) and ? 1 adrenoceptor antagonist prazosin (5, 15 ?g) or terazosin (5, 15 ?g) , respectively on the spinal analgesia of ketamine (100 ?g,ith) was studied. Results Dose dependent analgesia was observed following ith ketamine (100,200 ?g, P

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 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 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