Objective To investigate the effect of ketamine on lipopolysaccharide ( LPS)-induced activation of nuclear factor-kappa B (NF-kB) in rat lung in vivo.Methods Twenty-four adult Wistar rats weighing 260-310 g were randomly divided into four groups with 6 animals in each group : (Ⅰ) control group received normal saline (NS) 0.3 ml iv;(Ⅱ) LPS group received LPS 8 mg?g-1 in 0.3 ml of NS iv + LPS 100?g?kg-1 in 0.2 ml of NS introduced into trachea;(Ⅲ) ketamine group A received ketamine 4 mg?kg-1 in 0.3 ml of NS iv 30 min after LPS + ketamine 4 mg?kg-1 ip after an interval of 60 min; (Ⅳ) ketamine group B received ketamine 8 mg?kg-1 iv and ip instead of 4 mg?kg-1 in groupⅢ. The animals were sacrificed 240 min after NS or LPS injection and chest was immediately opened. 10 ml of blood was removed from left heart for determination of MDA and NO2 / NO-3 concentration. The NF-kB activation of nuclear protein extracted from the lung was measured by EMSA. 99Tc was used to determine the pulmonary vascular permeability.Results NF-KB activation in the lung, serum MDA and N0-2 / NO-3 and the pulmonary vascular permeability were significantly increased in LPS group as compared with those in control group (P

Obiective: To verify the effects of aminoguanidine on hemodynamics in sepsis.Method:Experiments were conducted in five groups of anesthetized dogs (each group n=8).In group 1,lipopolysaccharide (LPS)was injected intravenously, Group 2 received both LPS and L-arginine (300mg/kg)intravenously. Group 3 received both LPS and N-nitro-Larginine (L-NNA,20mg/kg) intravenously.Group 4 received both LPS and aminoguanidine (30mg/kg) intravenously. Group 5 received only saline. Hemodynamic and oxygenational data were measured or calculated. Extravascular lung water (EVLW)was measured. Result:L-arginine increased CI and decreased PVRI,while treatment with aminoguanidine without significant increased the BP,SVRI and PVRI.But all of untoward hemodynamic effcts of LPS were exacerbated by the addition of L-NNA,as DO_2 was significantly decreased by L-NNA,Therefore,though O_2ER was also increase (insufficiently),VO_2 was still decreased significantly.EVLW was markedly increased by LNNA. Conclusion:The No-selective inhibition with adiministration of aminoguanidine may have considerable value in the therapy of endotoxin shock.

Objective:To observe the effect of lidocaine on cerebral protection provided by retrograde cerebral perfusion. Method:Sixteen mongrel dogs underwent cardiopulmonary bypass and were cooled to 20 C. Circulation was then stopped and retrograde cerebral perfusion was carried out for 120 min,then CPB was resumed and animals were rewarmed to 36 C. Animals were divided into two groups:in lidocaine group(n=8),lidocaine was administrated continuously throughout the experiment (4mg/kg then 0.2mg?kg~(-1)?min~(-1) during cardiopulmonary bypass, 0.5mg/min during retrograde cerebral perfusion);in control group(n=8),normal saline was given at the same rate. Result:Cerebral tissue creatine phosphate and adenosine triphosphate concentrations and energy charge were significantly higher in the lidocaine group than those in the control group by the end of the experiment (creatine phosphate:2.44?0.53 versus 1.61?0.49?mol/g wet w,P

Objective To investigate the mechanism of electro-acupuncture (EA) at different frequency in improving synaptic plasticity injury in Alzheimer's disease(AD) rats, and to provide the theoretical basis for the clinical application of electro-acupuncture for the treatment of AD. Methods Ninety Wistar rats were randomly divided into normal group, model group, sham-operation group, and 2 Hz, 30 Hz, 50 Hz acupuncture groups, 15 rats in each group. AD rat model was established by injection of amyloid β1-42 (Aβ1-42) into the lateral ventricle. The rats in EA groups were treated with EA on Baihui and Shenshu acupoints at different frequencies (2, 30, 50 Hz). Learning and memory ability and space exploration ability of rats in each group were measured by Morris water maze test. The synaptic ultrastructure of hippocampus was observed by transmission electron microscopy. Nerve fibers were stained using Golgi techniques. The protein and phosphorylation levels of glycogen synthase kinase 3 beta (GSK-3β) in the brain tissues were detected by Western blotting method. Results(1) Compared with the normal group, the average escape latency time in the model group was significantly prolonged (P < 0.05), and the number of platform crossing was significantly reduced (P < 0.05), indicating that AD model had been established successfully. The average escape latency of rats in EA groups was significantly shortened and the frequency of platform crossing was increased as compared with those of the model group (P < 0.05). (2) The synaptic morphology of the hippocampus showed that the anterior membrane, posterior membrane and the interspace of the synapses in the model group were blurred, and the membrane structures of synapses were incomplete and dissolved. But the synaptic ultrastructures of the 3 EA groups were improved.(3) In the model group, the neurofibrillary tangles were found in the brain tissue, while the neurofibrillary tangles were relieved and the nerve fibers became clear in EA groups.(4) The levels of GSK-3β and GSK-3β(pTyr216) in the model group were significantly higher than those in the normal group (P < 0.05), whearas the GSK-3β(pSer9) level was significantly down-regulated (P < 0.05). In the EA groups, the levels of GSK-3βand GSK-3β(pTyr216) were down-regulated, while GSK-3β(pSer9) level was increased with the frequency of EA, and there was significant difference compared with the model group (P<0.05). (5) Compared with 2 Hz and 30 Hz EA groups, the number of plateau crossing, the average escape latency and the protein and phosphorylation levels of GSK-3β in 50 Hz EA group were significantly improved (P < 0.05). The improvement of synaptic morphology and neurofibrillary tangles of 50 Hz EA group was superior to that of the other 2 EA groups. Conclusion EA at different frequency can improve the learning and memory ability of AD rats, and the effect of 50 Hz is stronger. The therapeutic effect might be achieved by regulating the expression level of GSK-3βprotein and phosphorylation levels, which can improve synaptic plasticity damage of AD rats.

Objective: To evaluate the clinical profile of target controlled infusion based anesthesia using remifentanil and propofol. Methods: 16 ASA I II patients undergoing elective laparoscopic cholecystectomy were enrolled. Remifentanil was set at 7?g?L -1 as target and propofol at 3 mg?L -1 throughout the whole procedure. The hemodynamics during induction of anesthesia and recovery profiles were recorded. Arterial blood samples for analysis of remifentanil were taken 15min after infusion, 20 min after infusion and at time of emergence. Results: After induction of anesthesia, systolic blood pressure (SBP) decreased from (144?27) mm Hg to (101?18) mm Hg ( P 0.05). SBP, MBP and HR remained stable after intubation for 3min. No patient showed haemodynamic stress to tracheal intubation. Times from stopping administration of anesthetics until full spontaneous respiration, eye opening, tracheal extubation, orientation and discharging from the postanesthetic care unit (PACU) were (12?6), (9?4), (13?6), (15?5) and (19?7) min respectively. Measured drug values of remifentanil were (4.6?9.5) ?g?L -1 , (6.6?11.5) ?g?L -1 , (1.2?8.7) ?g?L -1 respectively. Conclusion: Remifentanil/propofol TCI based anesthesia achieved the optimal hemodynamic stability during anesthesia induction and maintenance, and better recovery profile from anesthesia. Measured drug values of remifentanil showed a considerable interindividual variation and more lower than the set target.

Objective To investigate the anti-apoptotic effect of gene A20 in treatment of trau-matic brain injury (TBI). Methods Thirty-five Sprague-Dawley rats were made severe TBI models and assigned randomly to experimental group and control group (35 rats in each group). After severe TBI, the rats in experimental group were injected with liposome-pcDNA3.1-A20 and those in control group injected with liposome pcDNA3.1-A20 at 30 minutes after severe TBI. The animals in both groups were sacrificed to remove the brain of five rats from each group at 12, 24, 48, 72 and 168 hours for sec-tioning. The expression of A20 and neurocyte apoptosis were defined by immunohistological method and TUNEL accordingly. The other ten rats were testified for neurological function at 1,2, 3 and 4 weeks af-ter TBI. Results The expression of A20 in experimental group was higher than that in control group, with statistical differences (P < 0. 01). The peak neurocyte apoptosis was found at 72 hours after TBI. The number of apoptosis cells in experimental group was lower than that in control group at 12, 24, 48 and 72 hours afte TBI (P < 0.01 or 0.05). At the 4th week after TBI, the neurological function in exper-imental group was better than that in control group (P < 0.05). Conclusion Gene therapy with A20 may have anti-apoptosis effect and exert neuroprotective effect on severe TBI.

Objective To determine whether lidocaine can improve the cerebral protection provided by retrograde cerebral perfusion. Methods Sixteen mongrel dogs were placed on cardiopulmonary bypass and cooled to 20℃. Retrograde cerebral perfusion was then carried out for 120 minutes, with the external jugular venous pressure kept at 3.33 kPa. Cardiopulmonary bypass was resumed, and the animals were rewarmed to 36℃. The animals were divided into two groups. In the lidocaine group (n=8), lidocaine was administrated continuously throughout the experiment. In the control group (n=8), normal saline was given at the same rate. Results In both groups, cerebral tissue creatine phosphate and adenosine triphosphate concentrations and energy charge increased by the end of hypothermic cardiopulmonary bypass, decreased continuously during retrograde cerebral perfusion, and recovered gradually after resuming cardiopulmonary bypass. Nevertheless, they recovered to significantly higher levels in the lidocaine group than in the control group (creatine phosphate: 2.44±0.53 versus 1.61±0.49 μmol/g wet weight, P=0.006; adenosine triphosphate: 0.71±0.18 versus 0.50±0.17 μmol/g wet weight, P=0.029; energy charge: 0.59±0.10 versus 0.48±0.09, P=0.044) by the end of the experiment. There was no significant difference between the two groups in the cerebral tissue water content (control group: 77.6%±1.9%; lidocaine group: 77.6%±1.3%).Conclusion Continuous lidocaine infusion accelerates the recovery of cerebral tissue high energy phosphate contents after resuming cardiopulmonary bypass, but it has no effect on the formation of cerebral edema after retrograde cerebral perfusion.

OBJECTIVETo investigate the biological characteristics of osteoblasts cultured in vitro from bone marrow (BM) of multiple myeloma (MM) patients and to explore their generation and osteogenic potential. Effects of some factors such as bortezomib and MM patient serum on the osteoblasts were observed.

METHODSTwenty MM patients and 10 healthy donors as controls were enrolled in this study. Osteoblasts from MM patients'BM were cultured in vitro. The generation and osteogenic potential of osteoblasts from MM patients and normal subjects were compared. The changes of their osteogenic potential and biological characteristics were observed. The antigens (CD34,CD138,CD45) on osteoblasts were catalyzed by flow cytometry. The levels of IL-7 were measured by ELISA. The BMP2 mRNAs were measured by RT-PCR.

RESULTSOsteoblasts from MM patients'BM could be cultured in vitro. The quantity of osteoblasts from MM patients (6.3±1.5) was less than normal subjects (8.2±2.6) (P<0.05). The osteoblasts cultured with MM patient serum (7.4±1.1) were less than those without patient serum (8.2±2.6) (P<0.05). Bortezomib increased those from MM patients after 6 days culture (8.9±2.1 vs 6.3±1.5) (P<0.05). Von Kossa staining showed that there were more calcium depositions in MM osteoblasts with bortezomib (8.8±1.9) than those without bortezomib (6.1±1.6) (P<0.05), but less than those from normal controls (15.8±2.2) (P<0.05). CD138, CD45, CD34 were not detected on the cultured cells. The level of IL-7 in MM patients'serum (2.07±0.71) was higher than that in normal controls (1.62±0.15) (P<0.05). The expression of BMP2 mRNA was seen in the normal osteoblasts and MM patients'osteoblasts cultured with bortezomib, but not be seen in those without bortezomib.

CONCLUSIONOsteoblasts could be cultured in vitro from MM patients' BM. The proliferation and osteogenic potential of osteoblasts from MM patients were decreased. Bortezomib was a positive regulatory of osteoblasts and MM patient serum was a negative one. They both could affect the proliferation and osteogenic potential of osteoblasts.

Adult ; Aged ; Bone Marrow Cells ; cytology ; Bone Morphogenetic Protein 2 ; metabolism ; Boronic Acids ; pharmacology ; Bortezomib ; Case-Control Studies ; Cell Differentiation ; Female ; Humans ; Male ; Middle Aged ; Multiple Myeloma ; blood ; Osteoblasts ; cytology ; Osteogenesis ; Pyrazines ; pharmacology ; Serum ; Tumor Cells, Cultured ; Young Adult