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Aim To investigate the role of TNF-αin propofol-induced neuronal apoptosis and long-term cog-nitive impairment in neonatal rats .Methods Seven-day-old SD rats were randomly divided into 3 groups:Control group ( n =12 ) , P ( single ) group ( n =6 ):propofol 50 mg · kg -1 was injected intraperitoneally (ip.)once;P(repeated) group(n=6):propofol 50 mg · kg -1 was injected ip.once daily, and for seven times. Hippocampal TNF-αlevel was measured 2 hours after propofol anesthesia , there were two time points(n=6) in Control group as control levels (post-natal day 7 for P ( single ) group and postnatal day 13 for P ( repeated ) group ) .In another experiment , 7-day-old rats were randomly divided into 5 groups:Con-trol group; P ( single ) group; P ( repeated ) group; P ( single ) +ETN group: ETN ( etanercept ) 0.4 mg · kg -1 was injected intracerebroventricularly 30 min be-fore propofol administration; P ( repeated ) +ETN group:ETN 0.4 mg· kg -1 was injected intracerebrov-entricularly 30 min before the 1st and 4th administration of propofol , which was injected ip .for seven times , once daily .Hippocampal neuronal apoptosis was detec-ted at postnatal day 7 [ P ( repeated ) and P ( repeated )+ETN groups not involved at this time point ] , 13, 21 and 35 , cognitive function was measured at postnatal day 36 to 41 using Morris water maze test .Results Propofol with different exposure times could increase hippocampal TNF-αlevels(P0.05 );in P ( repeated ) group, active caspase-3 positive neurons were more significantly increased at postnatal day 13, 21 and 35 than those in control group ( P0.05 ) .Con-clusion TNF-αmediates hippocampal neuronal apop-tosis and long-term cognitive impairment induced by propofol in neonatal rats , and long-term cognitive im-pairment may be related with persistent neuronal apop-tosis.
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Objective To compare landiolol and esmolol for treatment of intraoperative arrhythmia in dogs.Methods Experiment Ⅰ Eighty-eight KM mice (44 males, 44 females) , aged 4-6 weeks, were studied.The median lethal dose (LD50) and median effective dose (ED50) of landiolol and esmolol were determined using the sequential method.Treatment index (TI) was calculated.Experiment Ⅱ Eighteen dogs (9 males, 9 females), aged 8-12 months, weighing 7-10 kg, were equally and randomly divided into 3 groups: model group (group M) , landiolol group (group L) and esmolol group (group E).Intraoperative arrhythmia model was established by using gastrointestinal surgery combined with epinephrine.When sustained ventricular arrhythmias occurred, normal saline 0.5 ml/kg, landiolol 8.3 mg/kg and esmolol 10.0 mg/kg were given intravenously in C, L and E groups, respectively.The duration of arrhythmias was recorded.If bradycardia occurred (decrease in heart rate [HR] ≥ 25％ of the baseline value) , isoprenaline 0.05 mg/kg and atropine 0.03 mg/kg were injected intravenously.The occurrence of bradycardia after the initial administration of landiolol and esmolol, and the accumulated dose of landiolol and esmolol consumed when bradycardia occurred were recorded.Isoprenaline and atropine-induced improvement in bradycardia was recorded.Results Compared with esmolol, the LD50 and TI of landiolol were significantly increased (P＜0.01), and no significant change was found in ED50 of landiolol (P＞0.05).The duration of arrhythmias was significantly shorter in L and E groups than in group C, and in group L than in group E (P＜0.01).After the initial administration of landiolol and esmolol, the incidence of bradycardia was 0 and 100％, respectively, and the accumulated dose of landiolol and esmolol consumed when bradycardia occurred was (30± 13) mg/kg.Atropine could not effectively treat bradycardia, while isoprenaline could treat bradycardia.Compared with group L, the time for HR to rise and the duration for HR returning to the baseline value were significantly prolonged in group E (P＜0.05).Conclusion Compared with esmolol, landiolol provides faster improvement in intraoperative arrhythmia, weaker negative chronotropic effect, and higher safety;isoproterenol produces better efficacy in treating landiololinduced bradycardia in dogs.
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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 (P0 .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 .
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ObjectiveTo explore the effects and underlying mechanisms of acid sensing ion channels (ASICs) on pain behavior in a rat model of post-incision pain.MethodsFifty-eight adult male Sprague Dawley rats were used in this study,four rats were used for immunofluorescence test,thirty rats were employed for pain behavior test,and twenty-four rats were used for Western blot.Rats used for pain behavior test and Western blot were randomly divided into 3 groups:control group ( C group),incision pain model group ( I group) and amiloride group (A group).Plantar skin of rats in A group were infiltrated with 20 μl(200 μg)amiloride solution.Paw withdrawal mechanical threshold(PWMT) and paw withdrawal thermal latency(PWTL) of all rats in pain behavior test was tested at 24 h preoperative,2 h,4 h,8 h,12 h,24 h postoperative.Western blot was tested at 4 h postoperative.ResultsImmunofluorescence test displayed ASIC3 was expressed in plantar skin of all rats.The basal level of PWMT and PWTL of all rats in three groups was C group( (23.15 ± 5.10) g,( 11.32 ± 1.21 ) s),I group ( (23.26 ± 5.69) g,( 11.75 ± 2.01 ) s),A group ( (23.63 ± 4.96 ) g,( 11.47 ± 1.96) s) respectively,which was no significantly difference (P ＞ 0.05 ).PWMT and PWTL of I group and A group was significantly lower than that of C group at all time points postoperative (P ＜ 0.05) ; PWMT and PWTL of A group was at 2 h( ( 13.75 ±3.25)g,(9.96±1.32)s),4h((14.05±3.75)g,(9.17±2.11)s),8 h((9.75 ±2.74)g,(8.11 ±1.22)s)postoperative,which was significantly higher than that of I group (P ＜ 0.05 ).Compared with that of C group,the level of pERK1/2 expression was significantly increased in I group at 4 h postoperative (P ＜ 0.05 ),which could be inhibited by amiloride local infiltration (P ＜ 0.05 ).ConclusionASIC3 can mediate incision pain in a rat model of post-incision pain,through pERK1/2 signaling pathway,which can be inhibited by amiloride.
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ObjectiveTo investigate the role of the benzodiazepine receptor in the amnesic effect of propofol,etomicdate and ketamine in mice.MethodsTwo hundred and eighty-eight Kunming mice of both sexes weighing 18-23 g were randomly divided into 9 groups( n =32 each):gruup normal saline + normal saline (group NN); group normal saline+ fat emulsion (group NF); group flumazenil + normal saline (group FN); group normal saline + propofol (group NP) ; group flumazenil + propofol (group FP) ;group nomal saline + etomidate (group NE) ; group flumazenil + etomidate (group FE); group normal saline + ketamine (group NK) and group flumazenil + ketamine (group NK).Normal saline 10 ml/kg was given IP at 10 min before the tests,and normal saline 10 ml/kg,fat emulsion 10 ml/kg,propofol 25 mg/kg,etomidate 3 mg/kg and ketamine 20 mg/kg at 5 min before the tests in groups NN,NF,NP,NE and NK respectively.Flumazenil 1 mg/kg was given IP at 10 min before the tests,and normal saline 10 ml/kg,fat emulsion 10 ml/kg,propofol 25 mg/kg,etomidate 3 mg/kg and ketamine 20 mg/kg at 5 min before the tests in groups NN,NF,NP,NE and NK respectively.Darkness-avoiding test,platform-mounting test and Morris water maze test were performed to assess the cognition function.The latency of response and number of error were recorded in each test.ResultsPropofol,etomidate and ketamine significanfly shortened the duration of latency of response in platform-mounting test as compared with group NN.Etomidate also significantly increased the number of error in platform-mounting test as compared with group NN,while ketamine prolonged the duration of latency of response in Morris water maze test as compared with group NN.Flumazenil significantly counteracted the above action of the 3 intravenous anesthetics.ConclusionBenzodiazepine receptor may play an important role in the amnesic effect induced by propofol,etomidate and ketamine.
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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.
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Aim To observe the effects of promethazine on the analgesia,hypnosis,amnesia and therapeutic index of isoflurane.Methods The experiments were designed to study promethazine on the analgesic effect of isoflurane by hot-plate test and writhing test,and to study the effect of promethazine on the sleeping time of isoflurane by the method of righting reflex,and the amnesia of isoflurane by Morris water maze,and the ED_(50),LD_(50) by sequential method in mice.Results The result of hot-plate test and writhing test indicated that promethazine could enhance the analgesic effect of isoflurane(P＜0.05 or P＜0.01);through the experiment of righting reflex, sleeping time of isoflurane in mice was extended by promethazine(P＜0.01);in Morris water maze experiment, the average latency in the combination of promethazine and isoflurane was longer than that of the promethazine group or isoflurane group(P＜0.05 or P＜0.01), while aiming to the residence time, the combination of the two was shorter than that in the third quadrant(P＜0.01 or P＜0.05),the TCPP of the group of isoflurance was more than that of the combination group;promethazine could decrease the ED_(50) of isoflurance(P＜0.01),but it did not obviously affect its LD_(50)(P＞0.05).Conclusion Promethazine can not only reinforce the effect of isoflurance on analgesia,hypnosis and amnesia, but also boost the therapeutic index of isoflurance.
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Objective To investigate the effects of propofol injected into rostral ventromedial medulla (RVM) on nociceptive responses and examine whether GABA_A resceptor is involved in the mechanism. Methods Sixty-four pathogen free SD rats of both sexes aged 2-3 months weighing 250-300 g were randomly divided into 4 groups ( n = 16 each): group I control (group C) ; group Ⅱ propofol (group P) ; group Ⅲ bicuculline (group B) and group Ⅳ B + P (group BP) . The animals were anesthetized with intraperitoneal 1% pentobarbital 50 mg/kg. Their heads were fixed with stereotactic apparatus. An tracar was inserted into RVM for microinjection of propofol and/or bicuculline. The noxious responses were evaluated by hot plate test (response latency was measured) and formalin test (intraplantar injection of 2.0% formalin 100 μl) . Pain was scored (0 = no pain, 3 = severe pain) . Results Both hot plate test and formalin test showed that hyperalgesia was induced by microinjection of propofol into RVM. In hot plate test hyperalgesia induced by injection of propofol (4μg/0.4μl) into RVM was antagonized at 20 min after microinjection of bicuculline (10 ng/0.4μl) into RVM. In formalin test pain scores were significantly lower at 1, 5,10,20,30,40,50 and 60 min after intraplantar formalin injection in group BP than in group P.Conclusion GABA_A receptor in RVM partially mediates propofol-induced hyperalgesia.
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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.
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Objective To investigate the long-term effects of midazolam and penehyclidine hydrochloride on learning and memory function of mice.Methods According stratified random block design ,80 KM mice were divided into 4 groups: midazolam 1mg/kg(group M,n=20), penehyclidine hydrochloride 0.2mg/kg(group P,n=20),midazolam 1mg/kg + penehyclidine hydrochloride 0.2mg/kg(group M+P,n=20) and control group(group NS,n=20);20 mice in each group were divided randomly into testing memory acquisition(n=10) and memory consolidation(n=10) further.For behavioral testing a step-through passive avoidance test was used,in order to evaluate the effects of the agents administruted on the memory acquisition before fraining and on the memory consolidafion immediately after fraining.The step-through latencies and the numbers of errors 1,2,3,4,5,6 and 7 day after the training were recorded.Results Administration of midazolam impaired memory acquisition and consolidation when administrated alone or in combination with penehyclidine hydrochloride, and this effect persisted for 3 days . Administration of midazolam combinated with penehyclidine hydrochloride did not worsen the effect on memory acquisition,but worsen the effect on memory consolidation obviously. Furthermore, administration of midazolam combinated with penehyclidine hydrochloride impaired memory function persisting longer than that of administration of midazolam alone.Conclusions Administration of midazolam and penehyclidine hydrochloride as premedication was advantageous for prevention of awareness during operation, nevertheless was attributed to one of the causations of POCD.
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BACKGROUND: Quantitative pharmaco-electroencephalography (QPEEG) can reflect cerebral cortical function, which can be certainly affected by general anesthetics. Anesthesia depth has good correlation with the anesthetic dosage, so if we can find out the areas of brain and band of QPEEG which is relative to the anesthetic dosage, the band may be taken as the index to reflect the depth of anesthesia. OBJECTIVE: To observe the effects of propofol on the alpha2-band (α2- band) of QPEEG in rabbits. DESIGN: A randomized control animal experiment. SETTING: Jiangsu Provincial Key Laboratory of Anesthesiology, Xuzhou Medical College. MATERIALS: The experiment was carried out in the animal laboratory of Xuzhou Medical College from October 2004 to August 2005. Thirtysix healthy adult rabbits were randomly divided into propofol 2.5, 5 and 10 mg/kg groups with 12 rabbits in each, including 6 were used to observe the change of percentage of each band power of QPEEG, and the other 6 were used to observe the latency and duration for the disappearance of righting reflex in the rabbits. METHODS: The experiment was performed between 14:00-17:00 every day. Rabbits in the three groups were treated with intravenous injection of propofol of 2.5, 5 and 10 mg/kg respectively within 30 seconds. ① The conscious rabbits were fixed onto the platform in a prone osition, and the QPEEG was recorded with the method of power spectrum analysis before administration and at 20, 30, 40, 50, 60, 70, 80, 90, 100 and 110 s and 2, 5, 10, 15, 20 and 30 minutes after administration respectively. The sampling time for each time point was 5 s. ② The latency and duration for the disappearance of righting reflex in the rabbits were recorded. RESULTS: ll the 36 rabbits were involved in the analysis of esults. ① After the intravenous injection of propofol, the righting reflexes all disappeared within 1 minute. The greater the dosage, the shorter the latency and the longer the duration r=0.79, P ＜ 0.01). ② Compared with before administration, propofol of 2.5 mg/kg had no obvious influence on the percentage of α2-band power (P ＞ 0.05); The percentages of α2-band power in the brain areas were increased after administration in the propofol 5 mg/kg group (P ＜ 0.05); Except that there were no significant differences in the left and right parietal regions between the propofol 10 mg/kg group and the propofol 5 mg/kg group, the percentages of α2-band power in the other brain areas in the propofol 10 mg/kg group were decreased as compared with those before administration and those in the other two groups (P ＜ 0.05), and the changes above were more obvious in the frontal and temporal regions.CONCLUSION: The influence of propofol on the percentage of α2-band power of QPEEG is biphasic, it is suggested that α2-band would be an index to reflect the anesthesia depth of propofol.
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BACKGROUND: It is indistinct that whether ketamine can exert antinociceptive effect througb influencing the transmission of nocuous information in spinal cord; Nitric oxide (NO) in spinal cord participates mainly in the formation and development of hyperalgesia, and it can also induce Fos protein expression. It is still controversal whether it contributes to the transmission and mediation of ketamine to pain signal.OBJECTIVE: To observe the response to formalin stimulation in spinal cord of the rats and the effect of ketamine.DESIGN: Balanced randomized animal trial.SETTING: Department of Anesthesiology, Affiliated Hospital of Xuzhou Medical College; Jiangsu Provincial Key Laboratory of Anesthesiology.MATERIALS: This trial was carried out in the Jiangsu Provincial Key Laboratory of Anesthesiology, Xuzhou Medical College from January to March 2000. Totally 30 Sprague-Dawley rats were chosen and balanced randomized into 6 groups: formalin group (n=6), formalin + ketamine group (n=6), ketamine +formalin group (n=6), ketamine group (n=6), formalin+normal saline group (n=3) and normal saline group (n=3). The gender ratio was the same in each group.METHODS: Formalin group:The rats were stimulated for one hour by subcutaneous injection of 0.05 volume fraction of 200 μL in the center of palm of unilateral fore-claw. Formalin +ketamine group: The rats were stimulated for 10 minutes by formalin, then for one hour by intraperitoneal injection of 100 rg/kg ketamine. Ketamine + formalin group: The rats were injected with ketamine for 10 minutes, then with formalin for one hour. Ketamine group: the same dosage of ketamine was intraperitoneally injected into the rats for one hour. Formalin + normal saline group: The rats were stimulated for 10 minutes by formalin, then intraperitoneally given 10 mL/kg normal saline for one hour. Normal saline group: the same volume of normal saline was intraperitoneally injected into the rats for one hour.MAIN OUTCOME MEASURES: ① Behavioral performance of the rats in each group. ② Spinal sections were chosen, and stained with c-fos genetic immunohistochemical and NADPH-d histochemical methods. The changes of the number of Fos-like immuno-positive neurons (FLI) and FLI/nitric oxide synthase (NOS) double-labeled neurons in the 4-layer sections (layer Ⅰ -Ⅱ ,layer Ⅲ-Ⅳ ,layerⅤ-Ⅵ ,layer Ⅶ-X )of spinal dorsal horn of the rats were observed.RESULTS: All the thirty rats entered the stage of result analysis. ① Behavioral changes: The rats of formalin group and formalin+ normal salinegroup had apparent pain response; Several minutes after injection with ketamine, righting reflex disappeared and did not recover at perfusion period.Prolonged sleep was found without obvious pain response performance. ② FLI neuron expression: A lot of FLI positive neurons were found in the spinal dorsal horn of injec tion side of the rats in the formalin group and formalin+ normal saline group, and they distributed principally in the layer Ⅰ - Ⅱ of spinal dorsal horn.The distribution in the ketamine + formalin group and formalin + ketamine group was basically similar to that in the formalin group and formalin + normal saline group, but positive neuron counts were significantly reduced (P ＜ 0.01). ③ The expression of FLI/NOS double-labeled neurons: The number of double-labeled neurons in the spinal dorsal horn layer Ⅰ - Ⅱ of the rats in the ketamine+ formalin group and formalin+ ketamine group were significantly less than that in the formalin group and formalin+normal saline group [(1±1), (1±1), (7±3), (8±3),P ＜ 0.01].CONCLUSION: Some neurons of ipsilateral corresponding spinal segments participate in the transmission and mediation of pain signal. Ketamine can suppress the activities of these neurons and exert antinociceptive effect. The antinococeptive function of ketamine may be caused by the activity depression of the NOS-positive neurons in spinal cord.
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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.
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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
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0 05) group. Treatment with propofol or the combination of propofol and 5 HD delayed the onset of contracture during ischemia compared with control or 5 HD treatments for (6 4?2 1) min or (6 8?2 5) min vs (4 4?1 4) min or (4 2?1 6) min, respectively; P 0 05). The LVEDP in propofol or propofol plus 5 HD increased more slowly than in the control or 5 HD group. Maximal LVEDP occurred 17 min or 16 min,respectively after ischemia in the control group,whereas it occurred 20 and 22 min after ischemia in propofol and propofol plus 5 HD groups, respectively( P
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Aim To investigate the effects of midazolam and penehyclidine hydrochloride on learning and memory function of mice.Methods According to stratified random block design,80 KM mice were divided into 4 groups:midazolam 1 mg?kg-1(group M,n=20),penehyclidine hydrochloride 0.2 mg?kg-1(group P,n=20),midazolam 1 mg?kg-1+penehyclidine hydrochloride 0.2 mg?kg-1(group M+P,n=20)and control group(group NS,n=20),and 20 mice in every group were divided randomly into exper-iments of testing memory acquisition(n=10)and memory consolidation(n=10)further.To evaluate the behavioral alteration with these agents,a step-through passive avoidance test was used.Mice were administrated agents before training section for testing memory acquisition,and administrated agents immediately after training section for testing memory consolidation.The step-through latencies and the number of errors on 1,2,3,4,5,6 and 7 day after the training were recorded.Results Midazolam impaired memory acquisition and consolidation when administrated alone or in combination with penehyclidine hydrochloride.Administration of midazolam combinated with penehyclidine hydrochloride did not worsen the effect on memory acquisition,but worsen the effect on memory consolidation obviously.Furthermore,administration of midazolam combinated with penehyclidine hydrochloride impaired memory function persisting longer than that of administration of midazolam alone.Conclusion Administration of midazolam and penehyclidine hydrochloride would result in inhibiting learning and memory function of mice.
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Aim To investigate the relationship between neuronal nicotinic acetylcholine receptor and the amnesia and hypnosis induced by enflurane in mice.Methods Animal models were established by Intraperitoneal injecting of enflurane(2.2 ml?kg-1 and 0.4 ml?kg-1).Artificial cerebrospinal fluid or different dose of nicotine were intracerebroventricular injected,then sleeping time in the analeptic test was recorded;and the step down latency and error times in the step down test;step through latency and error times in the step through test.For the independent activity test,recorded the independent activity times of mice treated with enflurane(0.4 ml?kg-1) in 5 min.Results Compared with control group,intracerebroventricular nicotine decreased sleeping time in the analeptic test,increased step down latency and step through latency in both step down test and step through test.Furthermore,the error times were decreased in both tests.All the outcomes were significant and the influence was dose-dependent.There was no significant difference for the independent activity times of mice treated with 0.4 ml?kg-1 enflurane by ip injection.Conclusion All the evidence suggested that neuronal nicotinic receptor is one of important targets for the hypnotic and amnestic effect of enflurane in mice.
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Aim To study the effect of gamma-hydroxybutyric acid receptor(GHBR ) on neuronal apoptosis suffering from focal cerebral ischemia-reperfusion injury in rats. Methods The male Sprague-Dawley rats weighing 240～280 g were randomly divided into seven groups: sham operation group(sham), ischemia-reperfusion group(Isc/R) ,NCS-356 160、320、640 ?g?kg-1 group(N1、N2、N3),NCS-382 640+NCS-356 640 ?g?kg-1 group(NCS-382+N3),and nimodipine 600 ?g?kg-1 group(Nim).The middle cerebral artery occlusion(MCAO) model invented by Zea Longa with modifications was adopted. The experiment was divided into two parts after ischemia reperfusion for 24h:In the first part,we measured the cerebral expression of Bax, Bcl-2, Caspase-3 by immuneohistochemical method. In the second part,we measured neuronal apoptotic rate by flow cytometry in the ischemic cortex region. Results The expression rate of Bcl-2 and Bcl-2/Bax ratio of N1,N2,N3 and Nim groups were all higher than that of Isc/R group(P
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Aim To observe the effects of propofol at spinal level on nociceptive response in rats and the possible role of GABA_A receptor.Methods In the praxiology test,Sprague-Dawley(SD) female rats were randomized into groups.Bicuculline and propofol were microinjected into intrathecally(ith).The noxious response was evaluated with hot plate and formalin test.In immunohistochemistry test,Fos-like immunoreactivity(FLI) neurons expressed in spinal dorsal horn(DH) induced by formalin intraplantar injection(sc) of one hindpaw were used as a neuroactive marker to observe the effects of propofol on the noxious transmission in DH.Results In hot-plate test,significant analgesia produced by propofol(10 g?L~(-1)) was antagonized about 81%,55%,81% and 97% at 10,20,30 and 40 min by ith bicuculline(0.01 g?L~(-1),P
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0.05);in contrast, intrathecal NMDA 2.5,5,10 ng could significantly and dose dependently decrease the HPPT(P