Objective To observe the effect of ketamine on apoptosis and synaptophysin expression in 7-day-old infant SD rat hippocampal neural cells. Methods Thirty SD rats of 7 days old were randomly assigned to receive the injection of 25 mg/kg ketamine (K_ 1 group)or 50 mg/kg (K_ 2 group) or 50 ml/kg normal saline (K_ 0 group). In 24 h after injecton, all rats were killed and the synaptophysin was tested by using immunhistochemistry and Western blotting, the apoptosis of neuronal cell by Tunel. Results In 24 h after injection of ketamine,the number of apoptotic neural cells increased,which of K_ 0 group was (5.3?1.7), K_ 1 group (9.5?4.2), K_ 2 group (23.4?7.6), and the grey values of synaptophysin by immunhistochemistry of K_ 0 group was (174.11?4.68), K_ 1 group (181.36?4.17), K_ 2 group (198.25?3.06), and the OD values of synaptophysin piece decreased, which of K_ 0 group (4 007?758), K_ 1 group (2 621?465), K_ 2 group (987?183). Conclusion In 24 h after treatment with ketamine, the expression of synaptophysin was decreased in hippocampl neural cells, the number of apoptotic neuronal cells were increased, which may be involved in neurotoxicity caused by ketamine.

Aim To investigate influence of amitriptyline on glutamate-aspartate transporter(GLAST)in spinal cord of rats after spared nerve injury.Methods 60 male SD rats were randomly divided into 4 groups with 15 rats in each:control(A),SNI(B),amitriptyline(C),SNI+amitriptyline(D).Respectively 4 groups were treated with intraperitoneal injections of 0.2 ml saline(A and B),10 mg?kg-1 amitriptyline(C and D),bid.The L3～L6 segments of the spinal cord were isolated in 1,3 and 5 days after surgery.Expression of GLAST was determined by western blot and semiquantitative RT-PCR.Also,changes of mechanical withdrawal threshold(MWT)were measured.Results Compared to control,a markedly decreased MWT was showed in group B and the expression of GLAST at both protein and mRNA level increased firstly and decreased later.There were no changes of MWT in group C,but the expression of GLAST increased gradually.Rat MWT in group D did not change any more at the third days after surgery.In addition,the expression of GLAST in group D was higher than control group and kept stable.Conclusions Amitriptyline could increase the expression of GLAST,which may be one of its mechanisms in the treatment of neuropathic pain.

Objective To investigate influence of amitriptyline on astrocytic activation in spinal cord of rats after spared nerve injury(SNI).Methods A total of 120 male SD rats were randomly divided into 4 groups with 30 rats in each group:control(A),SNI(B),amitriptyline(C),and SNI+amitriptyline(D)groups,which respectively were treated with intraperitoneal injections of 0.2 ml normal saline(A and B),10 mg/kg amitriptyline(C and D),bid.The L3 to L6 segment of the spinal cord was isolated respectively at 1,3 and 5 d after surgery.Expression of glial fibrillary acidic protein(GFAP),marker of astrocytes,was determined by immunofluorescence,Western blot assay and semiquantitative RT-PCR.The changes of mechanical pain threshold were measured.Results Compared with control,group B had a markedly decreased rat mechanical pain threshold(P

Objective It has been shown that fluorinated inhalational anesthetics have various adverse effects on the lungs. The aim of this study was to investigate the effects of different concentrations of isoflurane (ISO) on the lungs in rats.Methods Ninety Wistar rats of both sexes weighing 140-200 g were randomly divided into two groups : (A) control group received only oxygen inhalation ( n = 30) and (B) isoflurane group (n = 60) which was farther divided into 2 subgroups (n = 30):0.6% and 1.4% isoflurane. In each subgroup isoflurane was inhaled for 2 h ( n = 10), 4h (n = 10) or 8 h ( n = 10) . The animals were placed in a glass container and isoflurane was delivered from ISO vaporizer into the container through the inlet. The end-tidal ISO concentration was checked at the outlet. The animals were sacrificed at the end of ISO inhalation. The lungs were immediately removed and blood was collected for determination of (1) lung water content, (2) protein content and neutrophil ratio in broncho-alveolar lavage fluid (BALF) , (3) serum and BALF surfactant protein-A (SP-A) content and (4) microscopic examination. Results There was no significant difference in all variables between control group and 0.6% ISO subgroup. Exposure to 1.4% ISO for 8 h caused an increase in neutrophil ratio and protein content in BALF, and serum SP-A content but a decrease in BALF SP-A content. There was no significant difference in lung water content between control group and 1.4% ISO (8 h) subgroup. Conclusion Isoflurane (1 MAC) inhalation over 8 h may impair the function of alveolar epithelium.

AIM To determine the effect of isoflurane(Iso) on pulmonary surfactant(PS) synthesis in cultured primary ATⅡ cells. METHODS ATⅡ cells were isolated from adult rat lungs and used for the experiments after 32 h in primary culture. Iso 0.28 and 2 8 mmol?L -1 was added into the media of normal and H 2O 2 (75 ?mol?L -1 )-treated cells, and the cells were further incubated for 2 h. The cell proliferation was measured with MTT method and PS synthesis with 3H-choline chloride incorporation. RESULTS Iso had no effect on the proliferation of ATⅡ cells, but markedly decreased PS synthesis in normal alveolar type Ⅱ cells, and aggravated the decrease of PS synthesis induced by H 2O 2. CONCLUSION Iso may decrease PS synthesis of alveolar type Ⅱ cells in vitro , and aggravate the damage of the cells under peroxidation condition.

To observe the effect of propofol on the change in neuron specific enolase(NSE) contents in the serum and cererospinal fluid(CSF) of rabbits suffering from brain injury, so as to explore the protective effect of propofol on the brain, 20 New Zealand rabbits were inflicted with brain injury and randomized into control group and propofol treatment group ( n =10 each). Samples of serum and CSF were collected before trauma and 4h, 24h, 48h, 72h and one week following trauma respectively. The contents of NSE in serum and CSF were measured by enzyme immunoassay (EIA) method. The results showed that the content of NSE in serum at 24h, 48h, 72h and one week, and that in CSF from 4h to one week after trauma in control group were elevated significantly as compared with those before trauma ( P

Objective To investigate the changes of alveolar epithelial permeability and the capacity of alveolar epithelium to remove alveolar fluid in the rat models of acute lung injury induced by oleic acid.Methods A total of 35 Wistar rats were randomly assigned to the control group(n=7),and the injured group(n=28) in which the lung injury was induced by intravenous injection of oleic acid at the dose of 0.25 ml/kg.The alveolar liquid clearance rate(ALCR),total lung water content(TLW),extravascular lung water content(EVLW) and alveolar epithelial permeability(AEP) were examined in 3,6,12,24 h after injury(n=7 at each time point).Results After lung injury,there was continuous increase of AEP,TLW and EVLW,as well as progressive reduction of ALCR.On 24 h after injury when all changes were most significant,AEP was increased by 68.7%,ALCR was reduced by 49.4%,TLW and EVLW increased by 44.6% and 92.0% respectively,as compared with control group.Conclusion The alveolar epithelial barrier might play a role in the pathogenesis of pulmonary edema in acute lung injury.

Objective To explore the effect of isoflurane on Na-K-ATPase activity in cultured primary alveolar type Ⅱ(ATⅡ) cells with or without being injured by H 2O 2.Methods ATⅡcells were isolated from adult rat lungs and incubated for 24h and divided into six groups. Group 1 served as control and received no treatment. Group 2 and 3 ATⅡ cells were exposed to 0.28 or 2.8mmol/L isoflurane. In group 4 cells were exposed to 75?mol/L H 2O 2. In group 5 and 6 cells were exposed to both 75?mol/L H 2O 2 + 0.28 or 2.8mmol/L isoflurane. Each group was incubated for another 2h after the addition of isoflurane and /or H 2O 2. The Na-K-ATPase activity of ATⅡcells ,the LDH activity and the MDA concentration of fluid culture medium were measured by biochemical methods.Results Isoflurane markedly decreased Na-K-ATPase activity in normal ATⅡ cells, but aggravated the decrease in Na-K-ATPase activity induced by H 2O 2. Isoflurane had no effect on LHD activity and MDA concentration of fluid culture medium of normal ATⅡ cells ,but significantly increased LHD activity and the MDA concentration of of fluid culture medium of ATⅡ cells injured by H 2O 2.Conclusions Isoflurane can inhibit Na-K-ATPase activity of ATⅡ cells in vitro, and aggravate the damage of ATⅡ cells caused by oxidants.

Objective Blood lactic acid(LA) and glucose(Glu) level are important parameters of anaerobic glycolysis and can be used to assess the severity of brain injury and cerebral metabolism. The purpose of this study was to evaluate effect of propofol on traumatic brain injury by measuring blood and CSF level of LA and Glu in addition to microscopic and NSE immunohistochemical examination of brain tissue. Methods Ninety New Zealand rabbits weighing 2.6-3.0 kg were used . Traumatic brain injury model was established according to Wang's method. Part Ⅰ . Twenty rabbits were divided into two groups of ten animal each. Blood and CSF samples were taken before and 4h, 24h, 48h, 72h and 1 week after trauma for determination of LA and Glu levels. Propofol group received propofol 30mg' kg-1?h-1 infusion for 30 min in addition to ketamine 1mg/kg before each collection of samples. PartⅡ . Seventy rabbits were divided into seven groups with ten animals in each group. Brain tissues were taken before and 24h, 72h, and 1 week after trauma for microscopic and NES immunohistochemical examination. Propofol group received infusion of 30 propofol mg kg-1 h-1 for 30 mm every day. In control group animals received same amount of normal saline. Results Blood and CSF levels of LA increased significantly after trauma in both groups but were significantly higher in control group than those in propofol group at corresponding intervals. Blood and CSF Glu levels decreased significantly in control group after trauma but in propofol group blood Glu level decreased only at 4h and 24h after trauma and CSF Glu level at 24h after trauma. There was significant difference in blood and CSF levels of Glu after trauma between the two groups. In both groups microscopic examination of brain tissue showed hemorrhage, degeneration, decrease in glial cells and vacuolization of some neuron in brain tissue of injured and surrounding areas at 24h after trauma, infiltration of neutrophils at 72h after trauma and cerebral interstitial edema and glial cell proliferation at 1 week after trauma. Neurons showed no NSE expression. In propofol group the above mentioned changes were relatively slight. Conclusions Propofol can significantly reduce blood and CSF LA levels after trauma and protect the animal from traumatic brain injury. Further studies are needed on the dosage and method of administration of propofol.

Objective To explore the change of alveolar epithelial liquid clearance capacity in lung edema following acute lung injury induced by oleic acid.Methods Forty-eight Wistar rats were randomly divided into 6 groups: the control(C), injury(I), amiloride(A), ouabain(O),amiloride plus ouabain(AO), and terbutaline(T) groups. Acute lung injury was induced with intravenous oleic acid 0.25 mlkg -1. 24h after injury, 5% albumin solution (5 ml?kg -1) was delivered into both lungs via the trachea in C and I groups. In A, O, AO and T groups, amiloride (2?10 -3 mol/L),ouabain (5?10 -4 mol/L), amiloride (2?10 -3mol/L) and ouabain (5?10 -4 mol/L)mixture and terbutaline(10 -4 mol/L),added respectively to the albumine solution,at 5ml.kg -1 were administered intratracheally to both lungs separately. One hour later, the alveolar liquid clearance rate(ALC), total lung water content(TLW), extravascular lung water content(EVLW) and arterial blood gases were measured.Results As compared with those in C group, severe hypoxemia, hypercapnia and acidosis appeared, ALC was reduced by 49.2% ,TLW and EVLW markedly increased in I group(P