Objective To determine the threshold of stroke volume variation (SVV) in determining the volume expansion responsiveness during fluid therapy in patients ventilated with different tidal volumes. Methods Fifty ASA Ⅰ or Ⅱ patients aged 20-75 yr undergoing elective gastrointestinal surgery under general anesthesia were randomly divided into 2 tidal volume groups (n = 25 each):group Ⅰ VT 8 ml/kg (group V1) and group ⅡVT 10 ml/kg (group V2). Radial artery was cannulated and connected to Vigelo monitor for continuous monitoring of cardiac index (CI), stroke volume index (SVI), systemic vascular resistance index (SVRI) and SVV. Internal jugular vein was cannulated for CVP monitoring. Anesthesia was induced with milazolam, propofol, fentanyl and rocuronium and maintained with intravenous propofol and remifentanil infusion. BIS was maintained at 40-50 during anesthesia. The patients were intubatel and mechanically ventilated (VT 8/10 ml/kg, RR 8-12 bpm, oxygen flow 2 L/min). 6％ HES 130/0.4 7 ml/kg was infused iv at a rate of 0.4 ml·kg-1 ·min-1 after induction of anesthesia. MAP, HR, CVP, CI, SVV, SVI and SVRI were recorded before and at 3 min after fluid therapy. The changing rate of SVV (△SVV) and CI (△CI) were calculated. The criterion for effective volume expansion was △CI 15%. The ROC curve for SVV in determring the volume expansion responsiveness was plotted and the diagnostic threshold was determined. Results ROC curve showed that the diagnostic threshold of SVV was 10.5 % in group V1 and 13.5% in group V2. The sensitivity and specificity in determining effective volume expansion were 93.3 % and 75.0 % in group V1 and 87.5 % and 85.7 % in group V2 respectively. The area under the curve for SVV and 95% confidence interval (CI) were 0.946 (0.860-1.031) in group V1 and 0.951 (0.868-1.034) in group V2. △SVV was negatively correlated with △CI in group V1 (=0.553) and V2 (= 0.602). Conclusion The threshold of SVV in determining the volume expansion responsiveness during fluid therapy is 10.5% and 13.5% in mechanically ventilated patients with tidal volume of 8 and 10 ml/kg respectively.

Objective To evaluate the effect of intrathecal ketamine on nitric oxide synthase (NOS)activity in the spinal dorsal horn via a rat model of sciatic constriction injury(SCI). Methods Thirty-six male SDrats weighing 160-180g were randomly divided into six groups(n = 6 in each group): group Ⅰ sham operation;group Ⅱ SCI; group Ⅲ-Ⅵ intrathecal ketamine + SCI. In group Ⅰ right sciatic nerve was exposed but noligature was placed around sciatic nerve. In group Ⅱ-Ⅵ four ligatures were placed around the right sciatic nerveand hed without obstructing the blood supply of the nerve. In group Ⅲ -Ⅵ ketamine 12. 5?g (group Ⅲ ),50?g(group Ⅳ ), 0?g (group Ⅴ ) or 300?g (group Ⅵ ) was given intrathecally 30 min before and 1,2 and 3 daysafer surgery. On the 7th and 14th day after operation thermal and mechanical hyperalgesia were measured with ice-cold water and von-Frey filaments. The animals were decapitated 14 days after SCI. The I_(4-6) lumbar spinal cordwas immediately removed and the spinal dorsal horn was dissected on ice and homogenized. The homogenate wascentrifuged at 3 500 r/min for 10 min and the protein content was determined. NOS achvity in the spinal dorsal hornwas measured using ultraviolet spectrophotometer. Results In group Ⅱ and Ⅲ pain threshold was significantlylowered and NOS activity significantly increased compared with those in group Ⅰ(sham operation) (P0 .05),but therewas signilicant difference in NOS activity between group Ⅱ and group Ⅳ, Ⅴ, Ⅵ (P

Objective To investigate the effect of intrathecal ketamine on the intracellular calcium ion concentration [Ca2+ ]1 in the spinal dorsal root ganglion (DRG) neurons in a rat model of chronic neuropathic pain produced by chronic constrictive injury (CCI) .Methods Thirty-six male SD rats weighing 160-180 g were randomly divided into 3 groups ( n = 12 each) : Ⅰ sham-operated group; Ⅱ CCI group and Ⅲ ketamine + CCI group. The animals were anesthetized with intraperitoneal pentobarbital 40 mg?kg-1 . The right sciatic nerve was exposed and 4 loose ligatures were placed on the trunk of the nerve at 1-2 mm interval. In sham-operated group (Ⅰ) the sciatic nerve was exposed but not ligated. Intrathecal catheter was implanted at L4,5 and correct placement was confirmed by aspiration of cerebro-spinal fluid. In group Ⅲ ketamine 1 mg ? kg-1 was administered intrathecally. 30 min before and on the 1st, 2nd, 3rd, 5th, 7th, 9th and 11th day after operation. In group Ⅰ and Ⅱ normal saline (NS) was given intrathecally instead of ketamine. Thermal and mechanical hyperalgesia were measured with ice-cold water and von-Frey filaments on the 7th and 14th day after operation. The animals were killed by cervical dislocation on the 7th (n = 6) and 14th ( n = 6) day. Bilateral DRG of L4-6 spinal nerve were removed and homogenized and centrifuged at 5 000 r/min. DRG neurons were isolated and [ Ca2+ ] i was measured by flow cytometry.Results In group Ⅱ (CCI) pain threshold to von-Frey hair stimulation decreased by 80.3% (on the 7th day) and 84.8% (14th day) while pain threshold to noxious thermal stimulation increased by 309.4% (the 7th day) and 336.2% (14th day) (P

Objective To investigate the effects of different target effect-site concentrations (Ces) of remifentanil on the sedative effect of propofol. Methods Fifty ASA Ⅰ or Ⅱ patients aged 20-55 yr weighing 48-86 kg with body mass index ＜ 30 kg/m2 were randomly divided into 5 groups ( n = 10 each) . Anesthesia was induced with TCI of remifentanil (Ce = 0, 2, 4, 6 and 8 ng/ml in groups R0-R4 respectively) and propofol. The initial Ce of propofol was 2.0 μg/ml in the 5 groups, and then the Ce of propofol increased by 0.5 μg/ml every 1 min until BIS value decreased to 50. BIS value and Ce of propofol were recorded as the patient lost consciousness. The effect-site concentration and consumption of propofol and the time required were recorded when BIS value decreased to 50.Results BIS value was significantly increased, while the effect-site concentration of propofol was significantly decreased as the patient lost consciousness, and the effect-site concentration and consumption of propofol were significantly decreased and the time required was shortened when BIS value decreased to 50 in R2-R4 groups compared with group R0 (P ＜ 0.05 or 0.01) . Conclusion The sedative effect of propofol can be enhanced when the Ce of remifentanil reaches 4 ng/ml, and the effects are comparable when the Ce of remifentanil reaches 4, 6 and 8 ng/ml.

Objective To investigate the changes in the expression of acid-sensing ion channel 3(ASIC3)in the dorsal root ganglion(DRG)in a rat model of bone cancer pain.Methods Twenty-four female SD rats,aged 3-4 yr,weighing 180-220 g,were randomly divided into 2 groups:sham operation group(group S,n =8)and bone cancer pain group(group P,n =16).Bone cancer pain was induced by intra-tibial inoculation of 10 μl Walker 256 cancer cell suspension in group P,while group S received intra-tibial inoculation of 5 μl normal saline.Body weight and paw withdrawal threshold to mechanical stimulation with yon Frey filaments(MWT)were measured at 0,1,3,5,7,9,1 1 and 14 d after cancer cell inoculation.The tibia was removed at 14 d after cancer cell inoculation in group S and at 7 and 14 d after cancer cell inoculation in group P for pathological and imaging examinations.The tumor cell growth and bony destruction were observed.The expression of ASIC3 in the DRG was determined by immunolluorescence.Results Pathological damage occurred at 14 d after cancer cell inoculation,bony destruction was observed obviously,ant cortical bone was missing in many places.Compared with group S,body weight at T3-7 and MWT al T2-7:were significantly decreaed,and the expression of ASIC3 was up-regulated at 14 d after cancer cell inoculation in group P(P ＜ 0.05).Conclusion Up-regulation of the expression of ASIC3 in the DRG is involved in the developntent and maiutenence ot bone cancer pain in rars.

Objective To investigate the changes in the expression of acid-sensing ion channel 3 (ASIC3)in the dorsal root ganglion (DRG) in a rat model of bone cancer pain.Methods Twenty-four female Sprague-Dawley rats,aged 3-4 weeks,weighing 180-220 g,were randomized into 2 groups:sham operation group (group S,n =8) and bone cancer pain group (group P,n =16).Bone cancer pain was induced by inoculating Walker 256 carcinoma cells into the medullary cavity of the left tibia,while group S received normal saline instead.The pain threshold was measured after determination of body weight on the day of inoculation (T0) and on 1,3,5,7,9,11 and 14 days after inoculation (T1-7).The tibia was removed for microscopic examination of the inoculated tibia and X-ray examination.The growth of tumor cells and damage to the tibia were observed.The expression of ASIC3 in the DRG was detected using immunofluorescence.Results The tumor cell infiltration occurred in the medullary cavity and bone destruction was observed in P group.Compared with S group,the body weight was decreased at T3-T7,and the pain threshold was decreased at T4-T7,and the expression of ASIC3 in the DRG was upregulated at T7 in P group (P ＜ 0.05).Conclusion ASIC3 protein expression in DRG is significantly up-regulated in the rats with bone cancer pain,suggesting that the pathway may be involved in the mechanism of bone cancer pain.

Objective To explore the feasibility of adding a flexible linker between two-pore-domain potassium channel TREK-1 (TWIK related K + channel 1)monomers to construct a tandem-linked dimer.Methods PCR was used to add a flexible linker between the two TREK-1 monomers.The cRNA obtained from in vitro transcription using the above vector was injected into Xenopus oocytes.After 24 -48 h,currents were recorded from these oocytes using a two-electrode voltage clamp.The effects of extracellular Ba2 + and pH on TdTREK-1 were observed and compared with those of native dimeric TREK-1.Results The tandem-linked dimeric TdTREK-1 was highly expressed in Xenopus oocytes.The currents through these channels were inhibited by extracellular Ba2 +and acidification.Furthermore,the responsiveness of the concatenated dimers to these extracellular stimuli was similar to that of native dimers.Conclusion Adding a flexible linker between the two monomers to construct the tandem-linked dimer does not affect the expression and gating properties of TREK-1, suggesting that the method be feasible.Such a method will allow the manipulation of a single subunit,which will help basis study the structure and function of TREK-1.

OBJECTIVETo investigate the role of muscarinic cholinergic receptor (mAChR) subtypes in the regulation of glutamatergic input to the spinal dorsal horn neurons and the possible mechanism.

METHODSWhole-cell voltage-clamp recordings on acute spinal slice was utilized to investigate the effect of activation of mAChRs and blockade of M2/M4 subtypes on glutamatergic synaptic transmission in rat spinal dorsal horn neurons.

RESULTSThe nonselective mAChRs agonist oxotremorine-M concentration-dependently decreased the amplitude of monosynaptic and polysynaptic evoked glutamate-mediated excitatory postsynaptic currents (eEPSCs) in most of the neurons. The M2/M4 antagonist himbacine completely blocked the inhibitory effect of oxotremorine-M in 92.3% of monosynaptic and 75% of polysynaptic neurons in the spinal cord slices. In the remaining 16% neurons, himbacine partially blocked the inhibitory effect of oxotremorine-M.

CONCLUSIONSActivation of mAChRs in the spinal cord attenuates synaptic glutamate release to the dorsal horn neurons mainly through M2 and M4 receptor subtypes, indicating that a presynaptic inhibition in the spinal cord may be involved in the regulation of nociception by the cholinergic system and mAChRs.

Animals ; Excitatory Postsynaptic Potentials ; Female ; Neurotransmitter Agents ; metabolism ; Posterior Horn Cells ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Muscarinic ; metabolism ; Synaptic Transmission

Objective To evaluate the efficacy and safety of domestic palonosetron hydrochlo-ride injection on its prevention of postoperative nausea and vomiting.Methods A multi-centered,ran-domized,double-blinded and placebo-controlled clinical trial was carried out.A total of 281 patients were enrolled,with 141 of patients in study group and 140 of patients in control group respectively. 0.075 mg of intravenous palonosetron hydrochloride injection was delivered in the study group before anesthesia induction.The drug was substituted by 1.5 ml of NS in the control group.All anesthesia inductions were conducted by the intravenous injection of propofol,fentanyl and rocuronium,and were maintained with sevoflurane and fentanyl.Complete remission rate and treatment failure cut-off time of vomiting were evaluated at 0-6 h,6-72 h,0-72 h postoperatively.Results In the study group CR% 0-6 h,6-72 h and 0-72 h were 107 (75.89%),104 (73.76%)and 92 (65.25%),the control group was 81 (57.86%),70 (50%)and 62 (42.86%),CR% of the study group was significantly higher than that of the control group (P <0.01).Insignificant statistical difference but significant clin-ical difference exists in their treatment failure cut-off time,386.5 min and 300.0 min,respectively be-tween the groups.Conclusion Domestic palonosetron hydrochloride injection is safe and effective in the prevention of postoperative nausea and vomiting.

Submandibular gland excision was performed on two patients using trans-oral robotic surgery (TORS). Complications such as the injury of marginal mandibular branch of facial nerve, ranula in the floor of the mouth, and postoperative hemorrhage were not observed. Visible cervical scar can be avoided and esthetic outcome can be expected by using this surgical modality.