Objective To investigate the effects of chronic inflammatory pain induced by injection of complete Freund' s adjuvant (CFA) into the plantar surface of hindpaw on the development of learning and memory and proenkephalin mRNA expression in hippocampus of neonatal rats. Methods sixty neonatal SD rats (6 rats from each of 10 litters) were randomly divided into control and chronic pain group ( n = 30; 3 rats from each of the 10 litters). In chronic pain group CFA 20 ? l was injected subcutaneously into plantar surface of left hindpaw on the 2nd day after birth whereas in control group normal saline 20 ? l was injected instead of CFA. Ten animals (1 rat from each of the 10 litters) in each group were killed on the 10th and 21st day after birth respectively. Hippocampi were removed for determination of proenkephalin mRNA expression by RT-PCR. Ten animals (1 rat from each of the 10 litters) in each group underwent Morris water maze test 3 times a day for 8 days starting from the 21st day after birth. Results The mean latent period before the rats found the hidden platform was significantly longer in chronic pain group than in control group. When the platform was removed the swimming time and distance of the rats in chronic pain group were significantly shorter than those in control group. There was no significant difference in the latent period before the rats found the visible platform between the two groups. The proenkephalin mRNA expression in hippocampus on the 10th and 21st day after birth was significantly lower in chronic pain group than in control group ( P

Objective To investigate the effects of chronic pain on spatial learning ability and the expression of neuronal cell adhesion molecules (NCAM) in hippocampus in neonatal rats.Methods Sixty newborn SD rats of both sexes were randomly divided into pain group ( n = 30) and control group ( n= 30). In pain group complete Freund' s adjuvant (CFA) 20 ?l was injected subcutaneously in the plantar surface of left hindpaw on the 2nd day after birth, whereas in control group normal saline 20 ?l was injected instead of CFA. The animals were weighed on the 3rd, 11th and 22nd day after birth. Ten animals in each group were anesthetized with intraperitoneal pentobarbital and killed on the 11th and 22nd day after birth respectively. The brains were immediately removed for determination of NCAM expression in CA3 and dentate gyms of hippocampus using immuno-histochemical staining technique. Morris water maze test was performed starting from the 21st day after birth for 8 consecutive days to assess the spatial learning ability ( n = 10 in each group) .Results The latent period before finding the hidden-plateform was significantly longer on the 1st and 4th day of the test (22nd and 25th day after birth) in pain group than in control group (P

Objective To observe the pain behavioral performance of rats that different sensory nerve fibers were transected,and examine the expression of brain-derived neurotrophic factor(BDNF) in these models.Methods Twenty-four rats were divided into three groups according to random number table method:SUR group,GS group and SHAM group, which received sural nerve transection, gastrocnemius-soleus nerve transection or sham operation respectively.There were 8 rats in every group.The expression of BDNF in the lumbar 5 DRG and spinal dorsal horn were detected,and the types of damaged cells were also observed.Results In GS group, 50% paw-withdrawal thresholds were significantly decreased on the ipsilateral hind paw compared with baseline and with those in SHAM group,and the paw-withdrawal durations in response to the thermal stimulus increased significantly (P＜0.01 ＝.In contrast, no change was found in SUR group(P＞0.05 ).The expression of BDNF in the lumbar 5 DRG ( (37.87 ± 4.23 ) % ) and spinal dorsal horn ( (21.9 ± 3.1 ) % ) was significantly higher in GS group than in SHAM group( ( 17.31 ± 2.12 ) %, ( 12.6 ± 1.3 ) % ), and no significant difference was found between SUR and SHAM groups(P＞0.05 ).FG opposite cells which also expressed BDNF in GS group were more than those in SUR group ( (47.7 ± 1.8) % and (26.7 ± 2.3 ) % ) (P ＜ 0.01 ＝.The percentage in N200 and FG double positive cells to N200 positive cells in GS group was significantly increased in GS group than those in SUR group ( (47.7 ±1.8 ) %, (26.7 ± 2.3 ) % ) (P ＜ 0.01 ＝.Conclusion The data suggest that injury of the sensory nerve innervating skin does not produce hyperalgesia, but injury of the sensory nerve innervating muscle does.Different kinds of neuron were damaged and the differences of BDNF expression is essential for this difference.

Objective To compare the effects of propofol versus isoflurane on brainstem auditory evoked potential (BAEP) and explore the difference in the effects of the two anesthetics on the brainstem. Methods Thirty ASA Ⅰ or Ⅱ patients aged 20-50 yr without heating disorder, scheduled for elective surgery performed under general anesthesia were randomly divided into 2 groups (n = 15 each): propofol group (group P) and isoflurane group (group Ⅰ). SpO2, PET CO2, BIS and BAEP were continuously monitored before and during anesthesia. Anesthesia was induced by propofol administered by TCI or isoflurane inhalation. Tracheal intubation was facilitated with vecuronium. The patients were mechanically ventilated. PET CO2 was maintained at 35-40 mm Hg and SpO2 at 98%-100%. After intubation BIS was maintained at 70 and 50 respectively ,the latency of the wave Ⅰ , Ⅱ and Ⅴ and the inter-peak latency (IPL) betwecn wave Ⅰ -Ⅲ , Ⅲ-Ⅴ and Ⅰ -Ⅴ were recorded.Results In group P there was no significant difference in the latency of the wave Ⅰ , Ⅲ and Ⅴ and the IPL between wave Ⅰ - Ⅲ , Ⅲ - Ⅴ and Ⅰ - Ⅴ between the baseline before anesthesia and at BIS 70 and 50. In group Ⅰ the latency of wave Ⅲ and Ⅴ and the IPL between wave Ⅰ - Ⅲ , Ⅲ - Ⅴ and Ⅰ - Ⅴ were significantly longer at BIS 50 than the baseline before anesthesia, while the latency of wave Ⅲ and Ⅴ and the IPL between wave Ⅰ -Ⅲ andⅠ -Ⅴ at BIS 50 were significantly longer than that at BIS 70. At BIS 50 the latency of wave Ⅴ and the IPL between wave Ⅰ -Ⅴ were significantly longer in group Ⅰ than in group P. Conclusion At comparable depth of anesthesia propofol exerts less depressant effects on BAEP indicating less depression of brainstem.

Objective: To explore the effects of ramipril, trimetazidine and the combination of ramipril and trimetazidine on renal cell apoptosis index (AI) and cytochrome C (Cyt-C) expression in experimental rats with chronic heart failure (CHF).
Methods: CHF model was established by partially banding of abdominal aorta superior to renal artery in experimental rats. A total of 50 male Wistar rats were randomly divided into 5 groups: Sham operation group, Model group, Ramipril group, Trimetazidine group and Combination (ramipril and trimetazidine) group.n=10 in each group. Renal tubular cell AI was examined by TUNEL method, mRNA and protein expressions of Cyt-C were detected by RT-PCR and Western Blot analysis in each group respectively.
Results: Compared with Sham operation group, Model group had increased AI of renal tubular cells, increased mRNA and protein expressions of Cyt-C,P<0.01. Compared with Model group, Ramipril group, Trimetazidine group and Combination group showed decreased AI of renal tubular cells (20.02 ± 1.14) %, (20.10 ± 1.2) % and (14.27 ± 1.40) % vs ( 40.82 ± 1.31) %; reduced Cyt-C mRNA expression (0.54 ± 0.06), ( 0.56 ± 0.05) and (0.44 ± 0.04) vs (0.89 ± 0.03); reduced Cyt-C protein expression (1.50 ± 0.11), (1.58 ± 0.12) and (0.75 ± 0.06) vs (2.53 ± 0.10); the most reduction was obtain by Combination group, allP<0.01.
Conclusion: Ramipril and trimetazidine can inhibit renal cell apoptosis and effectively improve the renal function in CHF rats. Combined medication is better than either of them alone.

Objective To determine the optimal dose of dexmedetomidine for intravenous analgesia after open radical resection of intestinal neoplasms when mixed with flurbiprofen axetil and butorphanol.Methods A total of 120 patients of both sexes,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,aged 20-60 yr,weighing 45-80 kg,undergoing elective open radical resection of intestinal neoplasms,were divided into 4 groups (n =30 each) using a random number table:control group (group C)and different doses of dexmedetomidine groups (group DEX1,group DEX2,group DEX3).Group C received flurbiprofen axetil 2 mg/kg and butorphanol 0.05 mg/kg for intravenous analgesia.In DEX1,DEX2 and DEX3 groups,dexmedetomidine 0.3 μg/kg was intravenously infused starting from 30 min before the end of surgery,and the analgesia solution contained dexmedetomidine 1,2 and 3 μg/kg,respectively,which was mixed with flurbiprofen axetil 2 mg/kg and butorphanol 0.05 mg/kg in 100 ml of 0.9％ normal saline,and the mixture was infused at a rate of 2 ml/h.Butorphanol 0.5 mg was intravenously injected as a rescue analgesic,postoperative pain was assessed using the visual analog scale at coughing,and visual analog scale score was maintained ＜4.The requirement for rescue analgesics was recorded within 48 h after operation.The occurrence of postoperative adverse reactions such as nausea and vomiting,respiratory depression,somnolence,bradycardia,hypotension and over-sedation,patient's satisfaction with analgesia and length of postoperative hospital stay were recorded.Results Compared with group C,the rate of rescue analgesia after operation was significantly decreased,and the degree of satisfaction with analgesia was increased in DEX2 and DEX3 groups,and the incidence of postoperative somnolence was significantly increased in group DEX3 (P＜0.05).No other adverse effects were found in DEX1,DEX2 and DEX3 groups.Conclusion When mixed with flurbiprofen axetil and butorphanol,the optimal dose of dexmedetomidine for intravenous analgesia after open radical resection of intestinal neoplasms is 2 μg/kg.

Objective To investigate the role of nitric oxide (NO) in the protective effects of morphine postconditioning against ischemia-reperfusion (I/R)-induced myocardial apoptoais. Methods Sixty pathogen-free SD rats were randomly divided into 4 groups ( n = 15 each) : group Ⅰ sham operation (S) ; group Ⅱ I/R; group Ⅲ morphine postconditioning ( M ) and group Ⅳ M + L-NAME ( non-selective NOS inhibitor). The animals were anesthetized with intraperitoneal pentobarbital 60 mg/kg, tracheostomized and mechanically ventilated. ECG was monitored. Right carotid artery was cannulated for BP monitoring and left jugular vein was cannulated for drug and fluid administration. Myocardial ischemia was induced by 45 min occlusion of left anterior descending coronary artery (LAD) followed by 120 min reperfusion. In group S LAD was exposed but not occluded; in group M morphine 1.25 mg/kg was injected iv over 5 min from 3 min before reperfuaion to 2 min of repeffuaion and in group M + L-NAME L-NAME 10 mg/kg was injected iv at 20 min before myocardial ischemia. Hemodynamic changes were monitored. The animals were killed at the end of 120 min reperfusion and their hearts removed. Myocardial apoptosis was determined by TUNEL technique. The expression of Akt phosphorylation was assessed by Western blotting. The NO content in myocardium was measured by a chemiluminescence detector.Results A large number of TUNEL positive cells (18.4 ± 1.1 ) % were observed in group I/R. Morphine postconditioning exerted a significant anti-apoptotic effect. The number of TUNEL positive cells was reduced to (10.8 ± 1.2)%. The myocardial eNOS phosphorylation expression and NO content were significantly increased in group M as compared with group I/R. The anti-apoptofie effect and increased NO production were significantly reversed by L-NAME. However, pretreatment with L-NAME did not inhibit the phosphorylation of eNOS in group L + M. Conclusion In vivo, morphine postconditioning can significantly reduce I/R-induced myocardial apoptosis through phosphorylation of eNOS and increase in NO production.

Objective To investigate the effect of morphine postconditioning on myocardial ischemiarepedusion(I/R)injury and the role of PI3K/Akt signaling pathway in the effect.Methods Seventy male SD rats weighing 280-330 g aged 16-17 weeks Were randomly divided into 5 groups(n=14 each):group Ⅰ sham operation(S);group Ⅱ I/R;group Ⅲ morphine postconditioning(M);group Ⅳ morphine postconditioning+ wortmannin(W+M);groupV wortmannin(W).Myocardial I/R injury wa.g produced by occlusion of anterior descending branch of left coronary artery for 45 min followed by 120 min reperfusion.In group M and W+M (groupⅢ,Ⅳ)morphine 1.25 mCkg was given iv at 3 min before and 2 min after reperfusion.In group W+M and W(groupⅣ,Ⅴ)wortmannin(a specific PDK inhibitor)15μ/gkg Was given iv at 20 min before ischemia. The animals were sacrificed at the end of 120 min repedusion for assessment of ischemic and infarct area and determination of total and phosphorylated Akt expression in myocardium by Western blot.Results There were no significant differences in the size of ischemic area and total Akt expression among the 5 groups. The infarct area was significantly smaller in group M than in group I/R. The were no significant differenees in the size of infarct area between group 1/R, W + M and W (group Ⅱ , Ⅳ,Ⅴ ). The phosphorylated Akt expression was significantly upregulated in group I/R and M as compared with group S, and was significantly higher in group M than in group I/R.Conclusion The PI3K/Akt signaling pathway activation is involved in the protective effect of morphine posteondifioning on myocardium against I/R injury.

An ultra-high performance liquid chromatography-tandem mass spectrometry ( UHPLC-MS/MS ) method was developed and validated for the simultaneous determination of 9 kinds of trace endocrine disrupting chemicals in biological samples using ultrasonic-assisted extraction followed by purification with gel permeation chromatography ( GPC) and silica gel columns. The sample extracts were purified by Bio beads S-X3 GPC columns with cyclohexane/ethyl acetate (1:1, V/V) as mobile phase, and the target compounds were eluted in the fraction of 12-28 mL retention volume. Electrospray ionization source operated in positive mode and atmospheric pressure chemical ionization source operated in negative mode were used for mass spectrometric detection. Data acquisition was carried out in multiple reaction monitoring mode. Recoveries were predominately within 65 . 2%-118 . 0%. Method quantification limits were 0 . 1-9 . 7 ng/g dw ( dry weight ) . This method was successfully applied to the analysis of the target endocrine disrupting chemicals in carps collected from the Pearl River. with the exception of carbanilide and triclocarban, the rest analytes were detected in fish tissue samples, with the concentrations varied within the range of 0. 1-22. 6 ng/g dw.

Objective To explore the effects of estrogen on oxidative stress of the lung tissue induced by acute paraquat (PQ) poisoning. Methods Thirty-two male adult New Zealand rabbits were randomly divided into model group and estrogen intervention group, 16 rabbits in each group. The model of lung injury induced by PQ poisoning was reproduced by feeding 16 mg/kg of 20% PQ through gastric tube. The rabbits in estrogen intervention group received intravenous infusion of 5 mg/kg estrogen after PQ challenge for 7 days, and the rabbits in model group received an equal volume of normal saline. Three rabbits in each group were sacrificed at 1, 2 and 3 days respectively after exposure. The lung tissue was harvested, the levels of reactive oxygen species (ROS) was determined by 2',7'-dichlorofluorescin diacetate (DCFH-DA), malondialdehyde (MDA) was determined by thiobarbituric acid (TBA), the mRNA expression of manganese-containing superoxide dismutase (MnSOD) was determined by reverse transcription-polymerase chain reaction (RT-PCR), and adenosine triphosphatase (ATP) content in mitochondrion was determined by enzyme linked immunosorbent assay (ELISA). The pathological changes in lung were observed under light microscopy using hematoxylin and eosin (HE) staining, and the lung injury was evaluated with lung injury score. Results The contents of ROS and MDA in lung within 3 days after PQ poisoning were gradually increased, and MnSOD mRNA expression and ATP content were gradually decreased. Estrogen intervention could significantly reduce the production of ROS and MDA after PQ poisoning [3-day ROS (fluorescence intensity): 161.05±30.04 vs. 188.30±31.80, 3-day MDA (mmol/L): 98.71±0.92 vs. 122.12±1.24], up-regulate MnSOD mRNA expression (integral A value: 3.05±0.90 vs. 1.22±0.24), and increase ATP content in mitochondrion (ng/L: 3.75±0.92 vs. 2.28±0.29) with statistically significant differences (all P < 0.01). In lung tissue after PQ poisoning, congestion, edema, focal pulmonary consolidation, pulmonary interstitial and alveolar space were infiltrated by a large number of neutrophil, alveolar interval were thickened obviously and the above phenomenon were most serious at 3 days after poisoning as shown under optical microscope. Estrogen intervention could significantly improve lung injury as compared with that of model group, and the lung injury score at 3 days was significantly lower than that of model group (11.8±0.7 vs. 13.5±1.0, P < 0.01). Conclusions The oxidative stress indicators in the lung tissue after PQ poisoning were obviously abnormal, the pathological damage was serious with time dependence. The administration of estrogen can reduce acute lung injury after PQ poisoning by reducing the oxidative stress.