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.

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.

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

Analgesic effect is the most important pharmacologic action of general anesthetics.The receptor mechanisms of analgesia of general anesthetics are complex,which may be related to GABAA receptor,NMDA receptor,glycine receptor,opioid receptor,nnAChRs and so on.In addition,other non-specificity mechanisms may also be involved.In this paper,the receptor mechanisms of analgesia of general anesthetics are reviewed.

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.

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.