B-7601.

Constant infusion, exponentially declining infusion and program infusion of theophlline were administered to rabbits byadopting the rabbit population pharmacokinetic parameters in this laboratory, and the plasma concentrations of the drug was measured by ul- traviolet spectrophotometry. The results showed that the plasma drug concentrations following exponentially declining infusion and program infusion attained the desired steady-state level at only 30 min, though the T1/2?= 6. 08h, The median absolute value of performance error in pro-gram infusion and exponentially declining infusion was 7. 8% and 14% respectively.

Objective To investigate the effects of isoflurane on cyclic adenosine monophosphate (cAMP ) content of brain in the rats. Methods Fourty SD rats were allocated randomly to 5 groups: no administration(control group,n=8), inhalation of 1.4% isoflurane until losing of righting reflex(loss of righting reflex group,n=8), inhalation of 1.4% isoflurane lasting 30 min(anesthesia group,n=8) ,righting reflex recovery after cessation of 30-min inhalation of 1.4% isoflurane (recoveryⅠ group,n=8) and 30 min after cessation of 30-min inhalation of 1.4% isoflurane (recovery Ⅱ group,n=8). The rats of each group were decapitated at the end of procedures to measure the cAMP content of brain tissue with competitive protein binding assay.Results As compared with that in control group,the cerebrocortical cAMP content only in anesthesia group significantly increased by 49% (P

Objective To determine the effects of isoflurane on the amino acid neurotransmitter contents in rat cerebral cortex, hippocampus and spinal cord. Methods Sixteen male SD rats weighting 220-280g were randomly divided into two groups: isoflurane group (A) and control group (B). Animals in group A were killed after 30min inhalation of 1.3% isoflurane and cerebral cortex, hippocampus and spinal cord were removed immediately for determination of glutamic acid (Glu), aspartic acid (ASP), glutamine (Gln), GABA and glycine (Gly) levels by high-performance liquid chromatography (HPLC), whereas in group B O2 was inhaled instead of isoflurane. Results As compared with control group, Asp and Glu levels in cerebral cortex and hippocampus decreased markedly while Gly level increased significantly in hippocampus and spinal cord in isoflurane group. Conclusions The inhibition of excitatory amino acid synapse transmission and augmentation of inhibitory amino acid synapse transmission may be involved in the mechanism of isoflurane anesthesia.

BACKGROUND:Tetramethylpyrazine (TMP) can inhibit the expression of vascular endothelial growth factor (VEGF), but it is uncertain that TMP inhibit the growth and proliferation of HL-60 leukemic cells induced by VEGF.OBJECTIVE:To observe the effect of TMP on the proliferation of HL-60 leukemic cells induced by VEGF.DESIGN:Repetitive measurement and observation.SETTING:School of Medicine, Wuhan University of Science and Technology.MATERIALS:The experiment was carried out in the Molecular Biology Laboratory Center, School of Medicine, Wuhan University of Science and Technology from March to June in 2007. Human leukemic cell line HL-60 cells were purchased from Shanghai Institute of Cell Biology. TMP hydrochloride injection was produced by Wuxi Seventh Pharmaceutical Products Limited (Lot number:011014), protamine sulfate injection was produced by Shanghai First Biochemical Pharmaceuticals (Batch number:010302), and immunohistochemistry kit was purchased from Boster company.METHODS:①Human leukemic cell line HL-60 cells at log phase were used for the experiments. Cells were treated with 100 μg/L VEGF, and then TMP at final concentrations of 1.5, 15, 150 mg/L was added into culture medium. While the cells in medium without TMP were taken as blank control group, and the cells in medium with 20 mg/L protamine as positive control group. Meanwhile cells without treatment of VEGF were served as VEGF control group. After cells were incubated for 48 hours, the growth inhibiting rate of HL-60 cells was detected by MTT assay.②After HL-60 cells were treated with TMP at the final concentrations of 1.5, 15, 150 mg/L for 24 hours, the protein expression of VEGF in HL-60 cells was examined by SP immunohistochemistry.MAIN OUTCOME MEASURES:①Growth inhibiting rate of HL-60 cells.②Protein expression of VEGF.RESULTS:①Growth inhibiting rate of HL-60 cells:After HL-60 cells induced by VEGF were treated with 15 and 150 mg/L TMP, the absorbance value was significantly lower than that in VEGF control group (P < 0.05).②Protein expression of VEGF:After HL-60 cells were treated with TMP for 24 hours, the protein expression of VEGF was down-regulated with increasing TMP concentration in a dependent manner. Significant differences were observed in the protein expression of VEGF between cells treated by TMP and the controls (P < 0.01).CONCLUSION:shRNA, by targeting hTERT mRNA, has no noticeable influence on growth and proliferation of hMSCs, and might be safe for the somatic cells which are normal but do not express hTERT.

BACKGROUND: It is indistinct that whether ketamine can exert antinociceptive effect througb influencing the transmission of nocuous information in spinal cord; Nitric oxide (NO) in spinal cord participates mainly in the formation and development of hyperalgesia, and it can also induce Fos protein expression. It is still controversal whether it contributes to the transmission and mediation of ketamine to pain signal.OBJECTIVE: To observe the response to formalin stimulation in spinal cord of the rats and the effect of ketamine.DESIGN: Balanced randomized animal trial.SETTING: Department of Anesthesiology, Affiliated Hospital of Xuzhou Medical College; Jiangsu Provincial Key Laboratory of Anesthesiology.MATERIALS: This trial was carried out in the Jiangsu Provincial Key Laboratory of Anesthesiology, Xuzhou Medical College from January to March 2000. Totally 30 Sprague-Dawley rats were chosen and balanced randomized into 6 groups: formalin group (n=6), formalin + ketamine group (n=6), ketamine +formalin group (n=6), ketamine group (n=6), formalin+normal saline group (n=3) and normal saline group (n=3). The gender ratio was the same in each group.METHODS: Formalin group:The rats were stimulated for one hour by subcutaneous injection of 0.05 volume fraction of 200 μL in the center of palm of unilateral fore-claw. Formalin +ketamine group: The rats were stimulated for 10 minutes by formalin, then for one hour by intraperitoneal injection of 100 rg/kg ketamine. Ketamine + formalin group: The rats were injected with ketamine for 10 minutes, then with formalin for one hour. Ketamine group: the same dosage of ketamine was intraperitoneally injected into the rats for one hour. Formalin + normal saline group: The rats were stimulated for 10 minutes by formalin, then intraperitoneally given 10 mL/kg normal saline for one hour. Normal saline group: the same volume of normal saline was intraperitoneally injected into the rats for one hour.MAIN OUTCOME MEASURES: ① Behavioral performance of the rats in each group. ② Spinal sections were chosen, and stained with c-fos genetic immunohistochemical and NADPH-d histochemical methods. The changes of the number of Fos-like immuno-positive neurons (FLI) and FLI/nitric oxide synthase (NOS) double-labeled neurons in the 4-layer sections (layer Ⅰ -Ⅱ ,layer Ⅲ-Ⅳ ,layerⅤ-Ⅵ ,layer Ⅶ-X )of spinal dorsal horn of the rats were observed.RESULTS: All the thirty rats entered the stage of result analysis. ① Behavioral changes: The rats of formalin group and formalin+ normal salinegroup had apparent pain response; Several minutes after injection with ketamine, righting reflex disappeared and did not recover at perfusion period.Prolonged sleep was found without obvious pain response performance. ② FLI neuron expression: A lot of FLI positive neurons were found in the spinal dorsal horn of injec tion side of the rats in the formalin group and formalin+ normal saline group, and they distributed principally in the layer Ⅰ - Ⅱ of spinal dorsal horn.The distribution in the ketamine + formalin group and formalin + ketamine group was basically similar to that in the formalin group and formalin + normal saline group, but positive neuron counts were significantly reduced (P ＜ 0.01). ③ The expression of FLI/NOS double-labeled neurons: The number of double-labeled neurons in the spinal dorsal horn layer Ⅰ - Ⅱ of the rats in the ketamine+ formalin group and formalin+ ketamine group were significantly less than that in the formalin group and formalin+normal saline group [(1±1), (1±1), (7±3), (8±3),P ＜ 0.01].CONCLUSION: Some neurons of ipsilateral corresponding spinal segments participate in the transmission and mediation of pain signal. Ketamine can suppress the activities of these neurons and exert antinociceptive effect. The antinococeptive function of ketamine may be caused by the activity depression of the NOS-positive neurons in spinal cord.

Aim To investigate the effect of spinal substance P on the antinociceptive propoties of ketamine. Methods Using behaviors and Fos expression technique,the effects of intrathecal administration (it) of substance P of different dose on the ketamine induced antinociception were observed in the formalin test of mice. Results Compared with NS group, the amount of time that mice spent licking the injected paw was dose-dependently decreased in 20 and 30 mg?kg -1 groups(P

AIM:To study the protective effects of penehyclidine hydrochloride(PHC) on transient forebrain ischemia reperfusion injury in gerbils.METHODS:The model of transient forebrain ischemia reperfusion was established in gerbils by bilateral carotid artery clamping.The effects of PHC on neurological function scores and the morphous of hippocampal pyramidal neuron of gerbils were observed after receiving transient forebrain ischemia reperfusion.SOD activities and contents of MDA in the hippocampus and cortex of gerbils were measured.RESULTS:In the groups of PHC(0.08),(0.24)(mg?kg~(-1)) and atropine,the stroke index was decreased,compared with the ischemia-reperfusion group after the gerbils received transient forebrain ischemia reperfusion for six hours.PHC could reduce the degree of injury in hippocampal pyramidal neuron after ischemia reperfusion for three days.CONCLUSION: PHC has protective effects on transient forebrain ischemia reperfusion injury in gerbils.