Objective:To explore causes of complicated acute lung injury (ALI) after percutaneous coronary interven-tion (PCI) .Methods:According to blood gas analysis and chest imaging examination ,a total of 175 patients under-going PCI were divided into ALI group (n=62) and non-ALI group (n=113) .High performance liquid chromatog-raphy was used to measure plasma concentrations of epinephrine (E) and norepinephrine (NE) during perioperative period .Plasma levels of interleukin-6 (IL-6) and procalcitonin (PCT) and chest CT imaging changes were meas-ured .Fluorescent immunoassay was used to measure plasma level of brain natriuretic peptide (BNP) to assess impact of cardiac function on ALI .Results:Compared with non-ALI group on 1d after PCI ,there were significant rise in plasma levels of NE [ (2.51 ± 0.31) nmol/L vs .(6.91 ± 0.39) nmol/L] and E [ (1.23 ± 0.11) nmol/L vs .(6.03 ± 0.37) nmol/L] ,P<0.01 all;and significant rise in plasma levels of IL-6 [ (119.81 ± 17.23) pg/ml vs .(252.28 ± 34.23) pg/ml] ,PCT [ (0.88 ± 0.01) pg/ml vs .(4.99 ± 0.87) pg/ml] and BNP [ (927.82 ± 89.72) pg/ml vs . (3936.55 ± 131.78) pg/ml] in ALI group (P<0.01 all) .Chest CT indicated that lung tissue inflammation was seri-ous .Conclusion:In patients undergoing percutaneous coronary intervention ,complicated acute lung injury is related to hyperactive sympathetic activity ,postoperative inflammation and heart function status etc .

0.05 ) ; propofol 500 /?mol?L-1 had dual effects : in 2/3 cells EPSCs were reduced to 67.5 % of the basiline values ( P

0.05). The EPSCs 10-40 min after LFS were 40.8% of the baseline (propofol group), 45.4% of the baseline (corticosterone group) and 25.4% of the baseline (propofol + corticosterone group) respectively, significantly lower than that in group Ⅰ and Ⅱ ( P

Objective To investigate the effects of propofol on the whole-cell excitatory postsynaptic currents (EPSC) and spontaneous excitatory postsynaptic current (sEPSC) in hippocampal CAl neurons.Methods Wistar rats (13-19 days old) weighing 40-60 g were decapitated and the hippocampi were immediately removed and placed in 0-4℃ artificial CSF aerated with 95% O2 and 5% CO2 . The hippocampi were sliced (400 ?m thick) . EPSCs were recorded in hippocampal CA1 neurons by stimulating the Schaffer collateral / commissural pathway. The 50 slices were divided into 5 groups (n = 10 each): group Ⅰ intralipid-1; group Ⅱ propofol-1; group Ⅲ SR95531 + propofol; group Ⅳ intralipid-2 and group Ⅴ propofol-2. In group Ⅰ, Ⅱ and Ⅲ after EPSCs were recorded for 10 min, 10% intralipid 90 ?l, 1% propofol 90 ?l (final concentration was 100 ?mol?L-1 and SR95531 10 ?mol?L-1 + propofol 100 ?mol?L-1 were added to the perfusate and again EPSCs were recorded for 40min. The changes in amplitude of EPSC were analyzed. In group Ⅳ and Ⅴ after the cell membrane was perforated and being stabilized for 10-15 min 10% intralipid 90 ?l and 1 % propofol (100 ?mol?L-1) was added to the perfusate and sEPSCs were recorded without stimulation. The holding potential was - 70 mV. Results Intralipid didn't affect EPSC but propfol 100 ?mol?L-1 reduced EPSC to 47.7% of the baseline value. SR95531 could reverse the effect of propofol on EPSCs. The frequency, amplitude and decay time of sEPSC in group propofol-2 were reduced to 31. 9% , 70. 9% and 50. 7% of those in group Ⅳ (intralipid-2) (P

Objective To observe the characteristics of macular optical coherence tomography (OCT) changes before and after silicone oil removal in patients who had undergone pars plana vitrectomy with silicone oil tamponade for macula-off rhegmatogenous retinal detachment (RRD).Methods Thirty-nine eyes that underwent silicone oil removal were enrolled in this retrospective study.The patients included 24 males and 15 females,with an average age of (53.05±4.03) years,the duration of silicone oil tamponade ranged from 3 to 7 months.Best-corrected visual acuity,intraocular pressure,slit lamp microscope and prelens,indirect ophthalmoscopy and fourier domain OCT were measured for all patients before and at months 1,3 and 6 after silicone oil removal.The macular microstructure were observed before and after silicone oil removal.Results Submacular fluid was detected in 6 eyes (15.38％),at the last time of follow-up,submacular fluid resolved completely in 2 eyes with disrupted ellipsoid zone,and resolved partly in 2 eyes.Disrupted ellipsoid zone were observed before silicone oil removal in 16 eyes (41.02％),6 eyes showed simultaneous disrupted ellipsoid zone and disrupted external limiting membrane,and there were 2 eyes that external limiting membrane was not identified,at the last time of follow-up,disrupted ellipsoid zone restored in 2 eyes and the extent of disrupted ellipsoid zone became reduced in 4 eyes.Cystoids macular edema were found in 2 eyes (5.12％),it resolved completely in 1 eye and resolved partly in 1 eye at the last time of follow-up.Macular epiretinal membrane was detected in 10 eyes (25.64％),and macular epiretinal membrane was found before silicone oil removal in 5 eyes,at the last time of follow-up,the membrane became thickened in 2 eye;5 eyes developed macular epiretinal membrane after silicone oil removal,at the last time of follow-up,the membrane became thickened in 1 eye.Secondary macular hole were noted in 2 eyes.Microcystic macular changes were observed in 9 eyes (23.07％),it was observed in 7 eyes before silicone oil removal,and was observed in 2 eyes after silicone oil removal,at the last time of follow-up,the cysts reduced in 1 eye.Conclusion Submacular fluid,disrupted ellipsoid zone and microcystic macular are the main macular ultrastructural changes that developed in patients with RRD before and after silicone oil removal.

Objective To evaluate the effects of propofol on apoptosis in the hippocampal neurons of fetal rats in vitro.Methods The isolated hippocampal neurons were seeded into 96-well plates or 24-well plates at a density of 5 × 104 cells/ml.The cells were randomly divided into 5 groups (n =18 each) using a random number table:control group (group C),in tralipid group (group Ⅰ) and propofol 1,10,100 μmol/L groups (P1-3 groups).In group Ⅰ,10％ intralipid was added to the culture media until the final concentration reached 100 μmol/L.In groups P1-3,propofol was added to the culture media until the final concentration reached 1,10 and 100 μmol/L,respectively,and the cells were then incubated for 3 h.The cell apoptosis was assessed by flow cytometry.The expression of Bcl-2 mRNA and caspase-3 mRNA was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).The expression of Bcl-2 and actived-caspase-3 protein was determined by Western blot analysis.The apoptosis rate was calculated.Results Compared with group C,the apoptosis rate was significantly increased,the expression of Bcl-2 mRNA and protein was down-regulated,and the expression of caspase-3 mRNA and actived-caspase-3 protein was up-regulated in P1-3 groups (P ＜ 0.05).There was no significant difference in the parameters mentioned above between group Ⅰ and group C (P ＞ 0.05).Conclusion Propofol induces apoptosis in isolated hippocampal neurons by inhibiting Bcl-2 expression and enhancing caspase-3 activity in fetal rats.

Objective To evaluate the effects of propofol on the intracellular calcium ion concentration ([Ca2+ ]i) and nuclear factor kappa B (NF-κB) activity in hippocampal neurons of fetal rats in vitro .Methods Ten pregnant Sprague-Dawley rats at 16-18 days of gestation ,were sacrificed and the fetal rats were taken out from the abdominal cavity .The hippocampal neurons of the fetal rats were isolated and seeded in culture plates .After being cultured for 9 days ,the neurons were divided into 7 groups ( n=12 each ) using a random number table :control group (C group) ,intralipid group (I group) and propofol 0.1 ,1 ,10 ,100 ,1 000 μmol/L groups (P1-5 groups) .In group I ,10% intralipid was added to the culture media until the final concentration reached 100μmol/L .In P1-5 groups ,propofol was added to the culture media until the final concentration reached 0.1 ,1 ,10 , 100 and 1 000μmol/L ,respectively .The cells were then incubated for 3 h .The [Ca2+ ]i and cellular morphology of hippocampal neurons were examined by laser scanning confocal microscopy before incubation with propofol and within 10 min after the end of incubation with propofol .The expression of NF-κB protein in the nucleus was detected at 7 days after the end of incubation with propofol by Western blot analysis to reflect NF-κB activity . Results Propofol increased [Ca2+ ]i in P2-4 groups ,while decreased [Ca2+ ]i in group P5 ( P<0.05 ) .Compared with group C ,the activity of NF-κB was significantly decreased in P1-5 groups ( P<0.05 ) ,while no significant change was found in C and I groups ( P>0.05 ) .The structure of hippocampal neurons was normal in C ,I and P1 groups .The branchings of axons and dendrites in hippocampal neurons were significantly decreased in P 2-4 groups , while the structure of hippocampal neurons became fuzzy , the cell membrane was destroyed and the axons and dendrites were not seen in group P5 .Conclusion Propofol can produce neurotoxic effects on hippocampal neurons of fetal rats by changing the [Ca2+ ]i and promoting NF-κB activation in vitro .

ObjectiveTo investigate the effects of propofol and etomidate on apoptosis in hippocampal neurons in rats.MethodsOne hundred and forty male 4 weeks old SD rats were randomly divided into 7 groups (n =20 each):control group (group C) ; groups P1,2,3 received intraperitoneal (IP) propofol 50,100 and 200mg/kg and groups E1,2,3 received IP etomidate 10,30 and 60 mg/kg respectively.Arterial blood samples were obtained at 2 h after the animals were fully awake for blood gas analysis.The animals were then sacrificed and their brains removed for microscopic examination of the ultrastructure of neurons in hippocampal CA1 area and detection of Survivin and Caspase-3 mRNA and protein expression in hippocampus by RT-PCR and Western blot analysis.ResultsThere was no significant difference in PaO2,PaCO2,SaO2,HCO3-,BE and pH value among the 7 groups.The neurons in CA1 area were basically normal in groups C,P1 and E1 while condensation of the chromatin of the nucleus and apoptotic bodies were observed in groups P3 and E3.Caspase-3 mRNA and protein expression was significantly up-regulated while Survivin mRNA and protein down-regulated in groups P3 and E3.Conclusion High dose of propofol and etomidate may induce apoptosis in hippocampal neurons in rats by up-regulation of Caspase-3 expression and down-regulation of Survivin expression.

Objective To evaluate the effects of propofol anesthesia on hippocampal protein kinase A (PKA)-cAMP response element binding protein (CREB) signaling pathway in neonatal rats.Methods One hundred and seventy-five male Sprague-Dawley rats,aged 7 days,weighing 8-15 g,were randomly divided into 5 groups (n =35 each) using a random number table:control group (C group) and propofol 25,50,100 and 200 mg/kg groups (P~ groups).Groups P1 and P2 received intraperitoneal propofol 25 and 50 mg/kg,respectively.Groups P3 and P4 received intraperitoneal propofol 100 and 200 mg/kg,respectively,and after righting reflex completely recovered,an increment of propofol 50 mg/kg was given until the total amount was finished.Five animals in each group were chosen and arterial blood samples were obtained immediately after the animals were fully awake for blood gas analysis.Five animals in each group were chosen at 2 h after fully awake and the age of 9 weeks,the rats were sacrificed and their brains were removed for microscopic examination of the ultrastructure of hippocampal neurons and for determination of PKA mRNA,CREB mRNA,PKA protein and pCREB protein in hippocampus (using RT-PCR and Western blot analysis).Results There was no significant difference in the indexes of blood gas analysis anong the five groups (P ＞ 0.05).Nuclear swelling and fragmentation,chromatin condensation,apoptotic bodies,decreased number of synapses and widened synaptic space were observed in P2,P3 and P4 groups.Compared with group C,the expression of PKA mRNA,CREB mRNA,PKA protein and pCREB protein was significantly down-regulated at 2 h after fully awake and the age of 9 weeks in P1,P2,P3 and P4 groups (P ＜ 0.05).Conclusion The mechanism by which propofol anesthesia induces neurotoxicity in neonatal rats may be related to inhibition of the activity of PKA-CREB signaling pathway.

Objective To investigate the effects of morphine on PTEN expression and NF-κB activity in human gastric carcinoma cell line MGC-803.Methods The human gastric cancer cell line MGC-803 was purchased from Cell Biology Research Institute,Chinese Academy of Sciences,and cultured in DMEM liquid culture medium.The cells were randomly divided into 2 groups(n = 6 each): control group and morphine group.The cells was exposed to 0.1 μmol/L morphine in morphine group.The apoptosis was assessed by flow cytometry after being incubated with morphine for 24 h.PTEN expression and NF-κB activity were detected using RT-PCR and Western blot.Results The apoptotic rate was significantly increased,PTEN expression was up-regulated and NF-κB activity was significantly decreased in morphine group compared with control group(P ＜ 0.05).Conclusion Morphine can promote the apoptosis in human gastric cancer cells by up-regulating PTEN expression and decreasing NF-κB activity.