Objective Propofol has profound influence on respiration. The purpose of this study was to evaluate the effect of propofol on respiratory mechanics during painless induced abortion. Methods Forty ASA Ⅰ women in early pregnancy (45-60 days) aged 17-52 yrs, weighing 42-80 kg undergoing induced abortion were enrolled in this study. Anesthesia was induced with intravenous 2.5 mg?kg-1 and maintained with intermittent i.v. boluses of propofol 30-50 mg. SpO2 and HR were monitored with Nellcor N-180 pulse oximeter. Respiratory mechanics was monitored with IFA-300 anemometer (TSI Co. USA) . The parameters measured included inspiratory / expiratory maximal air-flow velocity, inspiratory / expiratory mean air flow velocity, mean inspiratory and expiratory time, respiratory rate, inspiratory / expiratory air flow volume, dynamic inspiratory and expiraory airway pressure and indidence of apnea.Results SpO2 decreased significantly during maintenance of anesthesia with propofol. The mean and maximal inspiratory / expiratory airflow velocity and the inspiratory / expiratory airflow volume all decreased significantly during propofol anesthesia. The dynamic inspiratory / expiratory airway pressure significantly decreased during propofol anesthesia. The respiratory rate was significantly higher during propofol anesthesia while the mean inspiratory /expiratory time became shorter. Three patients developed apnea during induction of anesthesia with propofol (7.5%) . Spontaneous breathing returned within 1 min. Conclusion Spontaneous breathing is significantly depressed during propofol anesthesia in terms of respiratory mechanics. Care should be taken to maintain oxygenation and ventilation of the patient.

Objective The purpose of this study was to determine and compare the effect of patient controlled analgesia(PCA) with tramadol and fentanyl on postoperative sleep pattern in patients with severe obstructive sleep apnea syndrome(OSAS) Methods Forty five ASA Ⅱ patients with severe OSAS undergoing uvula palate pharyngoplasty(UPPP) were randomly divided into 3 groups of 15 patients each according to the postoperative PCA the patients received: 1) tramadol group; 2) fentanyl group and 3) control group The patients were premedicated with intramuscular atropine 0 01mg?kg -1 .The patients were adequately sedated (Ramsay Ⅱ Ⅲ) with midazolam 0 03 mg?kg -1 and fentanyl 2?g?kg -1 Awake intubation was performed under topical anesthesia Anesthesia was then induced with propofol 1 5 2 0 mg?kg -1 and maintained with inhalation of 1 0% 1 5% isoflurane and 60% N 2O and intermittent intravenous boluses of vecuronium PCA was started when the patients were awake Tramadol 500mg (tramadol group) and fentanyl 500?g (fentanyl group) were diluted to 100ml(tramadol 5mg?ml -1 , fentanyl 5?g?ml -1 ) A loading does of 10ml was given followed by continuous intravenous infusion at a rate of 3ml?h -1 PCA bolus does was 1 5ml and lock out time 10 min Polysomnography(PSG) was continuously monitored and recorded the first night after operation from 10 pm to 6 am next morning According to Rechtschaffen standard sleep was divided into 6 stages: stage Ⅰ, stage Ⅱ, slow wave sleep(SWS)(stageⅢ+Ⅳ), stageV (rapid eye movement REM) and stage Ⅳ(awake) Results During the 480 min of PSP monitoring, SWS was (13 06?7 56) min in tramadol group, (9 2?7 26) min in fentanyl group and (6 33?4 68)min in control group and the total sleep time (TST) was (197 4?84 48) min in tramadol group, (148 33?72 73)min in fentanyl group and (124 13?61 38)min in control group SWS and TST were significantly longer in tramadol group than those in control group(P

Objective To evaluate the effect of remifentanil on heart rate variability,to discuss the optimal does of remifentanil for tracheal intubation.Methods Thirty six ASA Ⅰ～Ⅱ patients were randomly assigned to one of three groups(n=12/group)according to the remifentanil target plasma concentration(2、4、6ng/mL).No premedication was given.The target-controlled infusion(TCI)of renifentanil was initiated 5 minutes after the TCI of propofol given at the target plasma concentration of 3.5?g/mL.Mean arterial pressure(MAP),heart rate(HR),HF,LF,HF/LF were measured from baseline values to 5 minutes after the operation began every minutes.MAP,HR,HF,LF and HF/LF were obtained on the time point as follows:before the induction(T0),before the start of remifentanil TCI(T1),before laryngoscopy(T2),and maximum values after intubation(T3),before operation(T4),maximum values after operation.All the data obtained were analyzed used ANOVA with SPSS 11.5 statistical software.P

Objective To investigate the effects of ketamine on the voltage-gated sodium channels in hippocampal pyramidal neurons, trying to elucidate the possible mechanism of general anesthesia with ketamine.Methods Hippocampal pyramidal neurons were isolated from Wistar rats of 2 weeks old. Whole-cell patch-clamp recordings were made from cultured hippocampal pyramidal neurons before and after the application of ketamine The effect of ketamine on the sodium current amplitude and the kinetics of the channel were studied. Results The sodium channels were reversibly inhibited by ketamine in a dose-dependent manner. IC50 of ketamine was (794?21) ?mol/L.The hyperpolarizing shift of both steady-activation and steady-inactivation was observed.Conclusion Ketamine inhibits the voltage-gated sodium channels to some degree. Sodium channel inhibition may be involved in the mechanism of general anesthesia induced with ketamine.

OBJECTIVE To observe the effect of clonidine on the proinflammtory cytokine and haemodynamics in hypoxia and trauma rats. METHODS Forty male SD rats were randomly divided into 5 groups: (A) hypoxia control group (n=8), (B) trauma control group (n=8), (C) hypoxia and trauma group(n=8), (D) hypoxia trauma clonidine precondition group (n=8), (E) hypoxia trauma colindine postcondition group (n=8). Except B group, the rats of each hypoxia group were placed in a sealed hypoxia chamber which O2 concentrate were maintained at (10 ?0.5)% for 6 days, 7h per day. Except A group, the rats of each trauma group received pharyngeal trauma after anesthesia. The rats in D and E group received clonidine 30 ?g/kg before 10 minutes or right after the pharyngeal trauma respectively. The mean artery pressure (MAP) and heart rate (HR) on the several moment around the trauma were recorded. The serum level of TNF-?, IL-6 was measured 1h after trauma. The tissues from lung and kidneys were taken to study the pathologic changes through microscope. RESULTS The MAP and HR raised obviously in each trauma group except D group on the trauma moment (P

Objective To investigate the effect of ketamine on the delayed rectifier outward potassium currents (IK) using whole-cell patch clamp technique. Methods Pyramidal neurons were enzymatically isolated from Wistar rat hippocampus. The effect of ketamine on the IK was assessed using whole-cell patch clamp technique. We measured the amplitude of the delayed outward rectifier IK by activating depolarizing pulse from -50 mV to 40 mV. Different concentrations of ketamine were added and potassium currents were measured. Results IK was inhibited by ketamine in a concentration-dependent manner. The five concentrations of ketamine (10, 30, 100, 300, 1000 ?mol/L) reduced peak IK currents by (10 ? 4)% , (19?4)%, (31 ?5)%, (50?7)%, (54?8) % respectively, with a mean IC50 of (100?18)?mol/L and Hill coefficient of 1.33?0.48. The V1/2 of activation curve was shifted from (1.82 ? 0.20) mV to (9.30 ? 1.03) mV (n = 8, P

Objective Propofol has been found to have anti-lipid peroxidation effect. We aimed to evaluate the effects of propofol on primarily cultured hippocampal neurons injured by glutamic acid. Methods Hippocampal neurons were obtained from newborn Wistar rats (within 24 h after birth) and cultured for 12 days. The 12 d cultured hippocampal neurons were randomly divided into three groups : (1) control group; (2) glutamate group in which cells were incubated with glutamate 100 ?mol?L-1 for 24 h; (3) propofol-glutamate group in which cells were incubated with propofol 500 ?mol?L-1 and glutamate 100 ?mol?L-1 for 24 h. Cell survival rate (MTT), apoptosis (flow cytometry) and C-fos protein (immuno-histochemistry) production were determined in each group. Results C-fos protein and apoptosis were significantly increased and survival rate was decreased in glutamate group compared with those in control group ( P

Objective To observe the effects of isoflurane on ocular hemodynamics .Methods Fifteen patients without eye diseases undergoing non-head and non-neck surgical procedures ,were enrolled in this study. Anesthesia was induced with intravenous propofol and atracuronium, followed by laryngeal mask insertion, and was maintained with isoflurane. Peak systolic velocity(PSV),end diastolic velocity(EDV),Tmax and resistant index(RI) of double ophthalmic arteries, central retinal artery and posterior ciliary arteries were determined by coloured Doppler imaging before anesthesia, 30 min following inhalation of isoflurane 1.0MAC or 1.5MAC respectively . Blood pressure, heart rate and SpO 2 were also measured at above time points.Results As compared with those before anesthesia ,no significant changes were found in all above parameters of double ocular arteries in all time points; PSV and EDV of central retinal artery decreased significantly with increase of isoflurane level(P005); all above parameters of posterior ciliary artery decreased significantly ,with increase of isoflurane level(P005). The diastolic pressure was positively correlated with PSV and EDV of central retinal artery and posterior ciliary arteries ,and negatively with RI , but no correlation to all above parameters of double ophthalmic arteries.Conclusions It may be dangerous for the patients with potential ischemia of eyes undergoing isoflurane anesthesia. Decreasing its concentration and improving blood pressure can increase ocular blood supply to prevent ophthalmic ischemic complications from occurrence.

Objective To study the role of NMDA-R system in the differential reaction of pain sense between peripheral inflamed local portion and distal portion Methods One hundred and forty-one adults Wistar rats were randomly divided into 6 groups The pain thresholds (PT) of bilateral feet were measured by paw-pressure technique NMDA receptor antagonist CGP378495mg?kg -1, NMDA receptor agonist NMDA 5mg?kg -1 or NS 1ml was injected intraperitonealy in the first three groups, respectively after one hindpaw was inflamed In the later three groups the same drugs were injected before one hindpaw was inflamed PT of bilateral feet in all groups were measured at virous times Results In the first three groups, PT of inflamed paw decreased ,and of non-inflamed paw increasedmarkedly after inflammation (P0 05), decreased significantly(P0 05), decreased significantly (P

Objective To evaluate the effects of different concentration of propofol on the anoxic response of primary cultured hippocampal neurons Methods Newborn (