Objective:To determine the influence of STOP(suction termination of pregnancy) with propofol anesthesia on stress hormone in the patients.Methods:Early pregnant patients of ASA Ⅰ-Ⅱ grade were divided randomly into two groups.The group C( n =32),as control group,received no anesthetic agent during STOP.The group P( n =34) was intervened with propofol anesthesia.BP,HR,So 2% were measured continuously during STOP.Blood samples were obtained from 66 patients at the following intervals:before STOP and 5min after STOP,and the plasma cortisol,blood sugar,insulin,C-peptide and growth hormone levels were measured.Results:The BP and HR decreased significantly during STOP and after STOP in group C compared with group P.The cortisol level in group C increased obviously aftr STOP.The significant difference in cortisol level was observed between two groups.Conclusion:STOP under propofol anesthesia could avoid the harm from the STOP syndrome and would not disturb the endocrine system of the patients.

0.05).Conclusion : Transfuse of 1000ml HES at perioperative stage could proliferate blood volume,and have mild influence on coagulation-fibrinolysis system without anaphylactoid reaction.It could be safely used at perioperative stage.

Objective To evaluate the changes in the expression of NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasomes in the spinal cord of rats with neuropathic pain.Methods Fifty-four healthy adult male Sprague-Dawley rats,weighing 250-300 g,were divided into 2 groups (n=27 each) using a random number table:sham operation group (S group) and neuropathic pain group (NP group).Neuropathic pain was produced by chronic constriction injury in anesthetized rats.The sciatic nerve was exposed,and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4.0 chromic catgut.The mechanical paw withdrawal threshold (MWT) was measured at 1 day before operation and 1,4,7 and 14 days after operation.After measurement of MWT at each time point after operation,the animals were sacrificed,and the L4_6 segments of the spinal cord were removed for determination of the expression of NLRP3,apoptosis-associated speck-like protein containing a CARD (ASC),caspase-1 and interleukin-1beta (IL-1β) protein and mRNA (by Western blot or by fluorescent quantitative real-time polymerase chain reaction).After measurement of MWT at day 14 after operation,the L4-6 segments of the spinal cord were removed for determination of the co-expression of NLRP3 with glial fibrillary acidic protein (GFAP) (by double immunofluorescence staining).Results Compared with S group,the MWT was significantly decreased,and the expression of NLRP3,ASC,caspase-1 and IL-1β protein and mRNA was up-regulated at each time point after operation in NP group (P＜0.05).The expression of NLRP3 and ASC protein and mRNA peaked at day 4 after operation,the expression of caspase-1 and IL-1β protein and mR-NA peaked at day 7 after operation,and the MWT reached the lowest value at day 7 after operation (P＜0.05).NLPR3 inflammasomes were mainly expressed in the astrocytes and neurons.Conclusion The expression of NLPR3 inflammasomes in the spinal astrocytes and neurons is up-regulated in the rats with peripheral nerve damage,and the change may be involved in the development and maintenance of neuropathic pain.

Objective To compare the low-intensity focused ultrasound (LIFU) and high-intensity focused ultrasound (HIFU) in treating pain due to chronic soft tissue injury.Methods Ninety-three patients with pain due to chronic soft tissue injury, aged 18-80 yr, with body mass index of 18-31 kg/m2,course of the disease 3 months-10 yr, and pain intensity of 4-8 in a numeric rating scale, were randomly divided into 2 groups using a random number table: low intensity group (group LI, n =49) and high intensity group (group HI, n =44).In group LI, the patients received LIFU with the minimum ultrasonic intensity causing senses (acid, hemp, swelling, pain) , and the treatment was continued for 10 min.In group HI, the patients received HIFU with the focused uhrasound intensity that could not be tolerated by the patients, the treatment was continued for 1 min each time and then suspended for 1 min, and the total time for treatment was 10 min.The patients received the treatment once a day, and the course of treatment was 5 days in both groups.When numeric rating scale score ＞ 4 during the treatment, parecoxib sodium 40 mg was injected intramuscularly as rescue analgesic.Both the therapeutic index and improvement in movement were used to evaluate the therapeutic effect, and the quality of life and depression were assessed and scored.The treatment-related adverse events were also recorded.Results The total effective rate was 98％ and 84％ in LI and HI groups, respectively.Compared with group HI, the total effective rate was significantly increased, the quality of life score was increased, and no significant change was found in depression score in group LI.No patients used parecoxib sodium or developed treatment-related adverse events in group LI.One patient (2％) required parecoxib sodium, the incidence of skin burns, nerve damage and abnormal pain was 4％, 2％ and 2％, respectively, and no patients developed tissue swelling in group HI.Conclusion LIFU has higher therapeutic effect than HIFU in treating pain due to soft tissue injury, and the safety is good.

Objective To evaluate the effect of celastrol postconditioning on focal cerebral ischemiareperfusion (I/R) injury in rats.Methods Sixty-four Sprague-Dawle rats (32 males,32 females),weighing 250300 g,were randomized into 4 groups using a random number table (n =16 each):sham operation group (group S) ; celastrol control group (group S + C) ; focal cerebral I/R group (group I/R) ; celastrol postconditioning group (group I/R + C).Focal cerebral I/R were produced by middle cerebral artery occlusion (MCAO).Dimethyl sulfoxide (DMSO) 0.3 ml/kg was injected intraperitoneally after shame operation in group S.Celastrol 3 mg/kg was injected intraperitoneally after shame operation in group S + C.DMSO 0.3 ml/kg was injected intraperitoneally at 5 min of reperfusion in group I/R.Celastrol 3 mg/kg was injected intraperitoneally at 5 min of reperfusion in group I/R + C.The neurologic deficit was scored at 5 min before reperfusion and 24 h of reperfusion.The infarct size was detected by TTC staining,and then the percentage of infarct size was calculated.The pathological changes in CA1 region of ischemic hippocampus were detected by HE staining.The activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX),content of reactive oxygen species (ROS) and expression of NOX1 and NOX2 mRNA (by RT-PCR) in ischemic brain tissues were detected.Results Compared with S and S + C groups,the neurologic deficit scores,infarct size,percentage of infarct size,NOX activity and ROS content were significantly increased,and the expression of NOX1 mRNA and NOX2 mRNA was up-regulated in I/R and I/R + C groups (P ＜ 0.01).Compared with group I/R,the neurologic deficit scores,infarct size,percentage of infarct size,NOX activity and ROS content were significantly decreased,and the expression of NOX1 mRNA and NOX2 mRNA was down-regulated in group I/R+ C (P ＜ 0.01).There was no significant difference in the parameters mentioned above between group S and group S + C (P ＞ 0.05).The pathological changes in CAl region of ischemic hippocampus were significantly attenuated in group I/R + C (P ＜ 0.01).Conclusion Postconditioning with celastrol can auenuate focal cerebral [/R injury in rats and inhibiton of oxidative stress response in brain tissues may be involved in the mechanism.

PONV (Postoperation nausea and vomiting) is one of the most possible problems after operation, and it has been a barraier to recovery of patients who had been orperationed, This review will focus on risk factors and prophylactic antiemetic therapy for PONV.

Objective To investigate the effect of parecoxib pretreatment on focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Sixty-four male SD rats weighing 250-300 g were randomly divided into 4 groups ( n= 16 each): sham operation group (group S); focal cerebral I/R group; focal cerebral I/R + parecoxib 5 mg/kg group (group P5); focal cerebral I/R + parecoxib 10 mg/kg group (group P10). Focal cerebral I/R was produced by occlusion of middle cerebral artery for 2 h followed by 24 h of reperfusion. Parecoxib 5 and 10 mg/kg were injected intravenously through the internal jugular vein 30 min before ischemia in group P5 and P10 respectively. The neurologic deficit scores (NDSs) were measured at 24 h of reperfusion and then the rats were decapitated.Brains were rapidly removed for determination of the infarct volume, apoptosis rate and expression of Bcl-2 and Bax. The ratio of Bcl-2 to Bax (Bcl-2/Bax) was calculated. Results The NDSs, apoptosis rate and expression of Bcl-2 and Bax were significantly higher, Bcl-2/Bax was significantly lower, and the infarct volume was significantly larger in group I/R than in group S ( P ＜ 0.01 ). The NDSs were significantly lower in group P10, and the apoptosis rate and Bax expression were significantly lower, the infarct volume was significantly smaller, Bcl-2 expression and Bcl-2/Bax were significantly higher in group P5 and P10 than in group I/R (P ＜0.05 or 0.01). The infarct volume was significantly smaller, the apoptosis rate and Bax expression were significantly lower, and Bcl-2 expression and Bcl-2/Bax were significantly higher in group P10 than in group P5 ( P ＜ 0.05 or 0.01 ). Conclusion Pretreatment with parecoxib can attenuate focal cerebral I/R injury in a dose-dependent manner through inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation of Bax expression in rats.

Objective To investigate the effects of hyperbaric oxygen preconditioning on cognitive function in aged rats after acute cerebral ischemia, and to analyze any changes in the cerebral cortex by magnetic resonance imaging (MRI). Methods Twenty-four aged male SD rats were randomly divided into a normal control group, a pure hyperbaric oxygen group, an ischemia group and an ischemia group preconditioned with hyperbaric oxygen. There were six rats in each group. A model of ischemia was induced in the ischemic group and the preconditioned ischemia group using a modified version of Pulsinelli's four-vessel occlusion method. The preconditioned ischemia group (before setting up the acute cerebral ischemia model) and the pure hyperbaric oxygen group were given hyperbaric oxygen treatment once a day for 5 days. Each group received axial line and coronal MRI scans in T1WI and T2WI. The rats' learning and memory abilities were evaluated with a Morris water maze, including escape latency and the percentage of swimming time in the platform quadrant. Results There was no obvious evidence of ischemic brain infarction in the normal control group or the pure hyperbaric oxygen group. There were clear arc-shaped bilateral cortex ischemic infarct areas in the ischemic group. The average ischemic infarct area in the preconditioned group was smaller than that in the simply ischemic group. Escape latency in the ischemia group was significantly longer than in the preconditioned group, and latency in the preconditioned group was significantly longer than that in the normal control and hyperbaric oxygen groups. The percentage of swimming time in the platform quadrant in the ischemic group was shorter than that in the preconditioned group, and that in the preconditioned group was shorter than those of the normal control group or the hyperbaric oxygen group. There was no significant difference between the normal control group and the hyperbaric oxygen group. Conclusions Continuous hyperbaric oxygen preconditioning can reduce the ischemic infarct area in aged rats after acute global cerebral ischemia and improve cognitive function.

Objective To evaluate the effect of spinal cord stimulation (SCS) on the expression of spinal substance P (SP) and calcitonin gene-related peptide (CGRP) in rats with neuropathic pain.Methods Forty-eight male Sprague-Dawley rats, aged 8 weeks, weighing 250-300 g, were randomly divided into 4 groups (n =12 each) using a random number table: sham operation group (S group) , n europathic pain group (group NP), sham electrical stimulation group (N-SCS group) , and SCS group.Neuropathic pain was induced by chronic constriction injury (CCI) in anesthetized rats.The sciatic nerve was exposed, and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 chromic catgut.Electrodes were placed into the epidural space at 5 days after CCI in N-SCS and SCS groups, and in addition, SCS was performed at 12-14 days after CCI in SCS group.The mechanical paw withdrawal threshold (MWT) was measured at 1 day before CCI, and 1, 4, 7 and 14 days after CCI.After measurement of pain threshold at day 14 after CCI, the animals were sacrificed, and the lumbar segments (L4-6) of the spinal cord were obtained for determination of the expression of SP and CGRP in the spinal cord by immunohistochemistry.Results Compared with group S, the MWT was significantly decreased, and the expression of SP and CGRP protein and mRNA was up-regulated in NP, N-SCS and SCS groups (P＜0.05).Compared with group NP, the MWT was significantly increased, and the expression of SP and CGRP protein and mRNA was down-regulated in group SCS (P＜0.05).Conclusion The mechanism by which SCS mitigates neuropathic pain may be related to down-regulated expression of SP and CGRP in the spinal cord of rats.

Objective To investigate the relationship between the mechanism of mitigation of neuropathic pain by spinal cord stimulation (SCS) and high mobility group protein box-1 (HMGB1)/Toll-like receptor 4 (TLR4)/NF-κB signaling pathway in the spinal cord of rats.Methods Forty-eight male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly divided into 4 groups (n =12 each) using a random number table:sham operation group (S group),chronic constrictive injury (CCI) group,sham SCS group (S-SCS group),and SCS group.Neuropathic pain was induced by CCI in the animals anesthetized with intraperitoneal chloral hydrate.The sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread.Electrodes were placed into the epidural space at 5 days after CCI in S-SCS and SCS groups,and in addition SCS was performed at 12-14 days after CCI in SCS group.Paw withdrawal threshold to mechanical stimulation (MWT) were measured at 1 day before operation and 1,4,7,14 days after CCI.After measurement of pain threshold at day 14 after CCI,the animals were sacrificed and the lumbar segments (L4-6) of the spinal cord were obtained for determination of mRNA expression of HMGB1,TLR4,and NF-κB p65 (in the nuclear protein,by real-time fluorescent quantitative PCR),protein expression of TLR4 and NF-κBp65 (by Western blot),and protein expression of HMGB1 (by immunohistochemistry).Results Compared with S group,MWT was significantly decreased after CCI,the mRNA and protein expression of HMGB1 and TLR4 was up-regulated,and the expression of NF-κB p65in the nuclear protein and mRNA was up-regulated in CCI,S-SCS and SCS groups.Compared with CCI group,MWT was significantly increased after spinal cord stimulation,the mRNA and protein expression of HMGB1 and TLR4 was down-regulated,and the expression of NF-κB p65 in the nuclear protein and mRNA was down-regulated in SCS group.Conclusion The mechanism by which SCS mitigates neuropathic pain may be related to inhibition of HMGB1/TLR4/NF-κB signaling pathway in the spinal cord of rats.