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 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.

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

AIM To investigate the effects of thiopental sodium on nitric oxide synthases (NOS) activity and nitride oxide (NO) in different rats cerebral synaptic membrane. METHODS Forty SD rats were divided randomly into five groups. The animals were injected introperitoneally (ip)thiopental sodium 30 mg?kg -1 or normal saline 10 ml?kg -1 (control group ) respectively. These rats were immediately decapitated before (induction group) and after (anaesthetic group) having disappeared righting reflex, and when righting reflex appeared again (recovery group), and completely conscious (awake group). In order to prepare synapsis, brain tissues were dissected on ice, then homogenized and centrifuged. NOS activity and NO was estimated by spectrophotometry. RESULTS Thiopental sodium 30 mg?kg -1 ip significantly inhibited NOS activity of cortex, brain stem and synaptic membrane as compared with that of normal saline group( P

Objective To investigate the effects of GABAA receptor agonist-muscimol and GABAA receptor antagonist-bicuculline on brain cyclic adenosine monophosphate (cAMP) content in rats undergoing isoflurane anesthesia. Methods Forty-eight SD rats of both-sexes weighing 200-250g were randomly divided into 6 groups: group I received intraperitoneal (ip) normal saline (NS) 10ml.kg-1 (control group); group II in which animals inhaled 1.4% isoflurane for 30 min, 30 min after NS ip (isoflurane group);group IE in which animals inhaled 1.4% isoflurane for 30 min, 30 min after muscimol Img-kg ip (muscimol + isoflurane group); group IV in which animals inhaled 1.4% isoflurane for 30min, 30 min right after bicuculline 8 mg.kg-1 ip (bicuculline + isoflurane group); group V received muscimol lmg. kg-1 (muscimol group); group VI received bicuculline 8mg.kg (bicuculline group). The animals were decapitated 1h after 30min isoflurane inhalation or intraperitoneal NS or muscimol or 5min after bicuculline ip (rats developed convulsion within 7 min after bicuculline ip) . Brain was removed immediately for determination of cAMP content of cortex or brain stem. Loss of righting reflex was taken as sign of anesthesia. Brain cAMP content was measured by competitive protein binding assay. Results Muscimol shortened the time of loss of righting reflex induced by isoflurane (P

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.