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Objective To investigate modulatory effects of Neb-SNP on inflammatory response and to explore the protection mechanisms of Neb-SNP in newborn piglets with ARDS. Methods Forty-five neonatal swines were randomly divided into five groups:group A (controlled group ,n = 9), group B (physiological saline group,n =9),group C (Neb-SNP 1 mg/ml,0. 9% NaCl, n = 9), group D (Neb-SNP 5 mg/ml,0. 9% NaCl, n = 9) and group E (Neb-SNP 10 mg/ml,0. 9% NaCl, n = 9). The pathological changes and activity of NF-κB in the lung tissue ,TNF-α ,IL-10 and IL-12 concentrations in serum at 30 minutes,60 minutes and 120 minutes after aerosol inhalation were observed. Results Activity of NF-κB and serum concentrations of TNF-α and IL-12 in the Neb-SNP treated group were lower than group B(P ＜0. 05) ,and serum IL-l0 concentration was obviously higher in the Neb-SNP group(P ＜0. 05). With an increase of Neb-SNP concentration,activity of NF-κB and serum concentrations of TNF-α and IL-12 were obviously increased, while serum concentrations of IL-10 was increased in group D and group E than that of group C (P ＜ 0. 05).Conclusion Inhalation of Neb-SNP reduced lung injury induced ARDS through lowering NF-κB activity and inhibiting expression of harmful inflammatory cytokines.
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BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells.OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2.DESIGN: A completely randomized controlled trial.SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing Medical University.MATERIALS: From January 2001 to October 2003, it was completed at the ICU of Children' s Hospital, Chongqing Medical University. Thirty male rats were selected and divided into sham operation group, ischemia group and nimodipine treated group randomly, with 10 rats in each group.METHODS: In sham operation group, the right common carotid artery was identified by blunt dissection without ligation under anesthesia in rats. In ischemia group, at 30 minutes before cerebral ischemia, 2 mL saline was injected intraperitoneally. In nimodipine treated group, at 30 minutes before cerebral ischemia, 0.2 g/L nimodipine (2 mg/kg) was injected intraperitoneally. In all the three groups, the duration between ischemia and decollation was 120 minutes. Rats were decollated under anesthesia and their brains were taken out to assess the activity of phospholipase A2, the free calcium level in brain cells, the brain water content and the changes in mRNA levels of type Ⅱ phospholipase A2 (secretive phospholipase A2) and type Ⅳ phospholipase A2 (cytoplasmic phospholipase A2) in brain tissue.pholipase A2) and type Ⅱ phospholipase A2 (cytoplasmic phospholipase A2)in brain tissue were measured in rats in all the groups.pholipsse A2 in brain tissue: In ischemia group and nimodipine treated group, the activity of phospholipase A2 were higher than that in sham operation group [(57.8 ±7.2),(42.5±6.1), (17.1±5.3)%, P＜ 0.05-0.01], and it was a litter lower in nimodipine brain cells: It was higher in nimodipine treated group and ischemia group than that in sham operation group [(775.8±105.5), (497.2±45.9), (103.8±10.3) μmol/L,P ＜ 0.05-0.01], and it was lower in nimodipine group than in ischemia group (P ＜ 0.01).that in sham operation group [(82.9±0.5), (80.0±1.1), (72.1±0.01)%, P ＜ 0.05-0.01], and it was lower in nimodipine treated group than that in ischemia group (Ppase A2 could be detected in brain tissue. And the mRNA level of type Ⅱ phospholipase A2 in brain tissue was very low. At 120 minutes after ischemia, mRNA of type Ⅱ phospholipase A2 was detectable and the expression of type Ⅱ phospholipase A2 was increased. Compared to ischemia group, the expression of type Ⅱ phospholipase A2 was not decreased in nimodipine treated group while the expression of type Ⅱ phospholipase A2 was decreased.CONCLUSION: Nimodipine is capable of decreasing the free calcium level in brain cells, the activity of phospholipase A2 in brain tissue and the brain water content after ischemia. However, it cannot significantly inhibit the expressions of type Ⅱ phospholipase A2 and type Ⅱ phospholipase A2 after cerebral ischemia.
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BACKGROUND: Free radicals are produced during ischemia, which can strengthen activity of lipid peroxidation; induce lesion of cell and cellular barrier, result in necrosis or apoptosis of neurons; and aggravate edema of ischemic cerebral tissue.OBJECTIVE: To observe the effects of polydatin (PD) on free radicals, lipid peroxidation, water contents and pathological morphology of brain tissue in rats with focal cerebral ischemia so as to explore its protective mechanisms.DESIGN: A randomized controlled trial.SETTING: Intensive Care Unit, Second Affiliated Hospital, Chongqing University of Medical Sciences; Pediatric Research Institute, Children's Hospital Chongqing University of Medical Sciences.MATERIALS: The experiment was carried out at the Pediatrics Medicine Institute of Chongqing Medical University from October 2001 to July 2002.Totally 48 healthy adult male Wistar rats were divided into 3 groups randomly,with 16 in each group. Group Ⅰ was sham-operated group: rats were anaesthetized, the right common carotid arteries were separated instead of being occluded. Group Ⅱ was ischemia group: to establish the right middle cerebral artery occlusion model of rats. Group Ⅲ was PD pretreatment group: polydatin (6 g/L, 12 mg/kg) were intravenously administrated 30 minutes before the onset of ischemia. Saline substituted for PD, besides, were intravenously administrated with the same way and dosage on Group Ⅰ, Group Ⅱ and Group Ⅲ.The rats were decapitated and the brains were immediately removed after cerebral ischemia 2 hours. In each group, 8 rats were chosen to be determined water contents of brain tissue, the other 8 rats were chosen to be determined levels of lipid peroxidation and free radicals in brain tissue.METHODS: According to the formula which was: wet weight-dry weight/wet weight×100%, water content of cerebral tissue was assayed. Superior liquid was taken to assay MDA with spectrophotometer thiobarbituric acid method (TBA) method, SOD activity assayed by xanthiue oxidase enzyme method, the activities of GSH-Px, CAT and NOS determined by colorimetry,the amount of protein determined by the method of Lowry. All the procedures were carried out strictly according to the instruction.malonaldehyde (MDA) and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and nitric oxide synthase chemia, contents of SOD, GSH-Px and CAT in cerebral tissue of PD group were obviously higher than those of ichemia model group [(226.43±8.69),(193.37±11.14) NU/mg; (244.38±12.34), (211.71±16.50) μkat/g; (59.85±9.67),water in cerebral tissue of PD group were obviously lower than those of ichemia model group [(6.38±0.54), (8.63±0.78) μmol/g; (78.72±0.43)%,tivity in ischemic tissue but the results were similar to that in ischemia model group [(12.00±1.00), (12.84±1.17) μkat/g, P ＞ 0.05] in brain tissue.ed that PD alleviated the ischemia edema of cerebral ischemia.CONCLUSION: PD can alleviate the reaction of lipid overoxidation, improve the activities of antioxidant-enxymes, reduce ischemia brain edema,protect the function of cell member, bring down the damage to ischemia neurons. It shows that PD has significant cerebral protective role on focal ischemia brain damage.
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0.05). The levels of ET-1 increased significantly in 1 h after CPB (P0.05). Conclusion The priming fluid with dexamethasone and aprotinin could inhibit the CBP-induced IL-6, TNF-?releasing, but have no such effects on ET-1, TXB 2 and 6-Keto-PGF 1? .
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Objective To evaluate the effectiveness of intratracheal tube suctioning by respiratory mechanics measurement.Methods The indexes of respiratory mechanics,including respiratory rate,expiratory tidal volume,% leak around the tube,dynamic respiratory compliance and mean airway resistance were measured just before and 20 minutes after intraendotracheal tube suction in mechanical ventilated children with respiratory failure.Results Fifty-two measurements was carried out in 11 patie nts.The mean values of respiratory risistance was (116.73±27.12)cmH2O/L.s before suctioning and (93.38±26.64)cmH2O/L.s after suctioning,with significant differrence(P＜0.01)；The mean values of % leak around the tacheal tube dereased from(18.12±4.12)% before suctioning to (8.71±3.76)% after suctioning (P＜0.05),The mean values of expiratory tidal valume was markedly increased from(7.31±2.12)ml/kg before suctioning to(5.72±1.2)ml/kg after suctioning(P＜0.01),The total respiraory rate markedly decreased after suctioning.Conclusion The respiratory mechanics measurement is very useful to evaluate the airway patient.The removal of secretions is crucial in respiratory managemet.