0.05);in contrast, intrathecal NMDA 2.5,5,10 ng could significantly and dose dependently decrease the HPPT(P

0.05).Inside experimental area,pain scores were decreased in both intradermal 0.25% lidocaine and saline injection group(P

Aim To investigate effects of calpain inhibitor calpeptin against hypoxia/glucose deprivation injury in rat hippocampal slices.Methods Forty hippocampal slices were randomly divided into two groups:Control group and calpeptin group.Calpeptin group then divided again into 1 ?mol?L-1 group,10 ?mol?L-1 group,100 ?mol?L-1 group and 200 ?mol?L-1 group according to the concentration of calpeptin in ACSF_ OGD(n=8 per group).By using electrophysiology method,changes of OPS and HIP during hypoxia/glucose deprivation process and effects of different concentration of calpeptin on it were observed.We also observed the neuronal apoptosis in hippocampal CA1 region after hypoxia/glucose deprivation and effects of different concentration of calpeptin on it.Results The HIP appearance rate and neuronal apoptosis in hippocampal CA1 region of 10 ?mol?L-1 group,100 ?mol?L-1 group and 200?mol?L-1 group significantly reduced,the OPS recovery amplitude and OPS recovery rate significantly increased,and every index among 10 ?mol?L-1 group,100 ?mol?L-1 group and 200 ?mol?L-1 group had no significant difference.Conclusion(10～200)?mol?L-1 calpeptin improved the hypoxia/glucose deprivation induced brain injury of rat hippocampal slices and the mechanism might be related to the inhibition of the neuronal apoptosis by calpeptin.

Objective To investigate the effectiveness of treating postherpetic neuralgia (PHN) by intradermal drug injection.Methods Ten rabbits of both sexes weighing 2.3-2.8 kg were anesthetized with intravenous urethane 1.5 g/kg. In group A (n = 5) 30% horseradish peroxidase(HRP) 500 ?l and in group B (n = 5) 1%-2% fluorescent nuclear yellow (NY) 500?l were injected intradermally at 6-8 points along the both sides of spine in the scapula region. After 48-72 h the animals were sacrificed and C4 -T10 spinal ganglia, cervical and thoracic sympathetic ganglia and celiac ganglia were harvested for identification of labeled neurocytes. Results Labeled neurocytes were found in C4-T10 spinal ganglia, cervical and thoracic sympathetic ganglia and celiac ganglia. There were more labeled neurocytes in the C6-T8 spinal ganglia. There were more labeled neurocytes in the sympathetic ganglia than in the spinal ganglia. The distribution of fluorescent labeled neurocytes corresponded to neurocytes labeled by HRP method. At the same segment there were more fluorescent labeled neurocytes than neurocytes labeled by HRP. Conclusion There is an ascending axoplasma streaming channel from nerver ending to the neurocytes in the ganglion as shown by morphological study and the good therapeutic effect of intradermal drug injection in the treatment of PHN may be related to this channel.

Objective To test the hypothesis that isoflurane-preconditioning (ISO-P) provides added protection of myocardium with hypothermia against ischemia-reperfusion injury through KATP channels. Methods Thirty-two SD rats of both sexes weighing 230-270 g were studied. The animals were anesthetized with intraperitoneal ketamine 100 mg?kg-1 and heparinized. Chest was opened and heart was immediately removed and perfused in a Langendorff apparatus with oxygenated (95% O2, 5% CO2) Krebs-Hensleit buffer (KHB) for 50 min,followed by 150 min of hypothermic-ischemia (perfusion was suspended and heart was immersed in 17℃ KHB) and 60 min of normothermic reperfusion (heart was again reperfused with 37.7℃ KHB and immersed in 37.7℃ KHB) (I/R). The animals were randomly divided into 4 groups of 8 animals:(l) control group; (2) ISO-P group; (3) ISO-P + GLB group and (4) ISO-P + 5-HD group. The control group received no pretreatment before I/R. In ISO-P group the heart was perfused with KHB gassed with 1% isoflurane for 15 min followed by 15 min wash-out before I/R. In group 3 and 4 the heart was perfused with KHB containing glibenclamide 20?mol?L-1 (group 3) or 5-hydroxydecanoate 150?mol ?L-1 (group 4) in addition to 1% isoflurane before I/R. Cardiac function was measured with a fluid filled latex balloon inserted in left ventricle (LVSP, LVDP, LVEDP, dp/dtmax, dp/dtmin). During hypothermic ischemia left ventricle pressure (LVP),S-time (the interval between the beginning of ischemia to the time point when LVP increased by 1 mm Hg from the baseline pressure) and C-time (the interval between the beginning of ischemia to the time point when LVP was lmmHg below the plateau pressure) were measured. Other criteria included coronary flow (CF),infarct size and creatine kinase.Results (l) S-time and C-time were negatively correlated with infarct size.(2)In ISO-P group (group 2) S-time and C-time were significantly longer during ischemia; LVDP and LVDP x HR were significantly higher during normothermic reperfusion and infarct size was significantly smaller than those in control group (groupl) (P

Objective To compare the effects of combined general-epidural anesthesia (CGEA) and general anesthesia (GA) on energy metabolism and oxygen cost of breathing.Methods Forty patients (25 male, 15 female) aged 42-61 yr weighing 42-75 kg scheduled for elective upper abdominal surgery were randomly divided into 2 groups : group CGEA (Ⅰ, n = 20) and group GA (Ⅱ, n = 20) . The patients were premedicated with midazolam 0.05 mg?kg-1 and scopolamine 0.3 mg i.m. . In groupⅠepidural catheter was placed at T9-10 A. test dose of 4ml of 2 % lidocaine was given. When the height of block was confirmed general anesthesia was started. In both groups anesthesia was induced with etomidate 0.3 mg?kg-1 , fentanyl 8 ?g?kg-1 and tracheal intubation was facilitated with atracurium 0.8 mg?kg-1 . Anesthesia was maintained with propofol in both group and intermittent epidural lidocaine in CGEA group and intermittent i. v. boluses of fentanyl in GA group. Muscle relaxation was maintained with atracurium infusion at 8 ?g?kg-1 ? min-1 during operation. Oxygen consumption ( VO2 ), CO2 production (VCO2 ) , energy expenditure ( EE) and respiratory quotient (RQ) were measured before anesthesia, during and after operation using indirect calorimetry (Datex, Deltatrac MBM-200) . Postoperative oxygen cost of breathing (OCB) was calculated during spontaneous breathing and controlled ventilation. Results VO2 , VCO2 , EE were significantly lower and RQ was significantly higher during operation than those before anesthesia in both groups (P

Objective It has been shown that protein kinase C (PKC), especially PKCy is involved in the nociceptive processing at the spinal level. This study was designed to investigate the effects of intrathecal (IT) morphine on PKCy immuno-reactivity in the spinal dorsal horn in a rat model of incisional pain. Methods Twenty-four male SD rats weighing 250-300 g were anesthetized with intraperitoneal pentobarbital 40 mg?kg-1. PE-10 catheter was inserted intrathecally to the lumbar region according to Yaksh. Five days later an incision of 1cm long was made in the plantar region of left hindpaw, parallel to the muscle under isoflurane anesthesia according to Brennan. The animals were randomly divided into 4 groups with 6 animals in each group : group Ⅰ sham-operation group received IT artificial cerebro-spinal fluid (ACSF) 20 ?l and 30 min later inhaled 1.4% isoflurane for S min but no incision was made; group Ⅱ received ACSF 20 ?l IT 30 min before incision was made; group Ⅲ post-incisional morphine group received morphine 5 ?g IT 30 min after incision and group Ⅳ pre-incisional morphine group received morphine 5 ?g IT 30 min before incision. The animals were sacrificed under general anesthesia 2 h after incision. The L4-5 segment of spinal cord was removed for determination of the expression of PKC? in the spinal dorsal horn by immuno-histochemical method.Results In group Ⅱ the PKC?-IR gray density in the spinal dorsal horn of the operated side was significantly higher than that of contralateral side and that in group Ⅰ( P

0.05) compared to control group. Conclusion Induction of anesthesia with isoflurane or enflurane decreases the number of NOS positive neurons in the 6 nuclei in limbic system. The changes in NOS positive neurons in limbic system may be involved in the mechanism of isoflurane and enflurane anesthesia.

Objective To investigate the effect of hypothermia on cytokine expression in rats with lipopolysaccharide- induced acute respiratory distress syndrome (ARDS), and investigate whether or not hypothermia can inhibit inflammatory reaction and attenuated lung injuries, thereby preventing the development of ARDS. Methods A rat model of ARDS was established by intratracheal instillation of lipopolysaccharide (3 mg/ kg, 0.5 ml, LPS) at 16 h after LPS (1 mg/kg, 0.3 ml) intraperitoneal administration. Thirty-two male Sprague Dawley rats were randomly divided into four groups: ARDS + Normalthermia (AN) , ARDS + Hypothermia (AH) , NS+ Normalthermia (NN), and NS + Hypothermia (NH) groups. At 3 h after ARDS, rats were killed by hemorrhage from carotid artery. Lung lavage was performed, tumor necrosis factor ?(TNF-?) , interleukin-6 (IL-6) concentrations in BALF were measured using enzyme-linked immunosorbent assay (ELISA) .Results Within (2.3?1.6) h the ARDS model in AN group and AH group was successfully replicated. Compared with the NN group, the concentrations of TNF-? and IL-6 increased significantly in the AN group ( P 0.05). Conclusion Hypothermia has inhibitory effect on the expression and release of the pro-inflammatory cytokine (TNF-?, IL-6) in rats with ARDS. Hypothermia may inhibit inflammatory reaction, attenuated lung injuries and serve as a new measure to prevent and treat ARDS.

Objective To investigate the effects of moderate hypothermia on the permeability of alveolar capillary membrane in acute lung injury (ALI) induced by lipopolysaccharide (LPS) .Methods Thirty-four adult male SD rats weighing 300-350g were randomly divided into 4 groups: control group (n = 8) ; LPS group (n = 10); hypothermia group (n = 8) and LPS + hypothermia group (n = 8) . The animals were anesthetized with intraperitoneal (i.p.) 1% pentobarbital 30 mg?kg-1, intubated and mechanically ventilated (RR 80 bpm, VT 20 ml?kg-1, I: E 1:2) . Right external jugular vein and left carotid artery were cannulated for BP and CVP monitoring and blood sampling. ALI was induced by LPS 1.0 mg?kg-1 i.p. and 16h later, intratracheal instillation of LPS 1.5 mg?kg-1. ALI was considered established when PaO2/FiO2 ≤300. Hypothermia was induced by surface cooling. Body T0 was reduced to 32.5-33.0℃. In control and hypothermia groups normal saline was given instead of LPS. Arterial blood samples were taken for blood gas analysis and MAP and CVP were recorded before (T0, baseline) and 1, 2, 3, 4 h after ALI (T1-4) . At the end of experiment (4h after ALI was established) the animals were killed by exsanguination. The lungs were removed. Lung lavage was performed and the concentration of albumin in bronchoalveolar lavage fluid (BALF), the left lung wet/dry weight ratio, myeloperoxidase (MPO) activity of lung tissue were measured. Lung tissue was also taken for histologic examination by transmission electron microscopy.Results There was no significant difference in hemodynamics among the 4 groups. PaO2/FiO2 and PaCO2 remained unchanged in the control group and hypothermia group. PaO2 /FiO2 was significantly decreased and PaCO2 was significantly increased as compared to the baseline values (T0) in LPS group (P