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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.
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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.
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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
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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.
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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