AIM: To observe the effect of aminoguanidine (AG) on hemodynamics and lung capillary permeability in acute lung injury (ALI) in rabbits. METHODS: 24 rabbits were equally divided into four groups: saline group, endotoxin group, AG group and AG plus endotoxin group. In AG plus endotoxin group, endotoxin was injected to animals to make an ALI model, 25mg/kg AG was injected following that and let this sustain 3 hours. Meanwhile, mean arterial pressure (MAP), mean pulmonary arterial pressures (MPAP) and blood gas analyses were observed during this period. At the end of the experiment, broncho-alveolus lavage was performed, pathologic samples were treated routinely and lung wet weight/dry weight ratio was calculated. RESULTS: After endotoxin injection, MAP and arterial oxygen pressure (PaO 2) decreased, and MPAP increased significantly. The injection of AG had little effect on MAP, but AG could markedly decrease MPAP and increase PaO 2. Cell count in broncho-alveolus lavage fluid (BALF) was less in AG plus endotoxin group than in endotoxin group. Although AG did not affect total protein in BALF, low molecular weight proteins decreased in AG plus endotoxin group by the assay of electrophoresis. Tissue wet weight/dry weight ratio also decreased in this group. Pathologic study showed that there were fewer inflammatory cells and less lung edema in AG plus endotoxin group. CONCLUSION: AG could improve hemodynamics status and attenuate acute lung injury induced by endotoxin in rabbits. [

AIM: To examine whether calcitonin gene-related peptide (CGRP) enhances nitric oxide (NO) level in pulmonary circulation blood and observe the influence of CGRP on mean pulmonary artery pressure (mPAP) in rabbits with acute lung injury (ALI) caused by oleic acid. METHODS: The level of NO was assessed by measuring the presence of nitrite in cervical artery blood by the Griess reaction, mPAP was measured with right ventricular catheter. RESULTS: The level of nitrite in cervical artery blood was significantly increased and the mPAP was markedly reduced after administration of CGRP intravenousely.CONCLUSION: CGRP enhanced the NO level of pulmonary circulation blood and reduces the mPAP significantly in rabbits with ALI.

Objective To evaluate the ability of goblet cell in the airway in rat with asthma to synthesize granulocyte-macrophage colony-stimulating factor (GM-CSF),and the role of calcium-activated chloride channel (CLCA) in the synthesis. Methods A model of asthma was replicated in male BALB/c mice with ovalbumin sensitization. The goblet cells in small bronchi were identified with AB-PAS staining,and the expression of GM-CSF in the same airway was assessed with immunohistochemistry staining. The recombinant plasmid of pIRES2-EFGP/hCLCA1 was transfected stably into the human mucoepidermoid cell NCI-H292. The expression and transcription levels of GM-CSF in transfected cells were determined with immunohistochemistry staining and RT-PCR assay. The non-transfected cell and the transfected cell exposed to niflumic acid (NFA),which was a CLCA inhibitor,were designated as two control groups. Results Positive staining of GM-CSF expression could be seen in the goblet cells of small bronchi. The cells with expression of hCLCA1 showed much higher levels of GM-CSF expression and transcription than those of two control groups. It was also found that NFA could effectively reduce the levels of GM-CSF in transfected cells. Conclusion The goblet cell of asthmatic airway can synthesize GM-CSF,and one of mechanisms is the increased expression of CLCA.

Objective To investigate the optimal dose of remifentanil combined with dexmedetomidine for awake tracheal intubation.Methods 60 cases with difficult airway general anesthesia surgery from March 2014 to August 2016 in Jinhua People's Hospital were selected and divided into group R1,R2,R3,20 cases in each group.0.6μg/kg dexmedetomidine 10 minutes micro pump intravenously,Simultaneous target-controlled infusion effect of the chamber concentration of remifentanil.2.0ng/mL remifentanil in group R1,2.3ng/mL remifentanil in group R2,2.5ng/mL remifentanil in group R3.All patients underwent full surface anesthesia with 2％lidocaine under visual soft mirror guidance.The heart rate(HR),mean arterial pressure(MAP)and Ramsay sedation score at before anesthesia(T0),at the end of the administration(T1),intubation(T2),immediately after intubation(T3),tracheal catheter placement reaction score and record tracheal intubation during respiratory depression,cardiovascular adverse events,postoperative follow-up of tracheal intubation process satisfaction.Results MAP,HR and RR at T2,T3 in group R1 were significantly higher than those in group R2 and R3,the difference was statistically significant(P<0.05).The incidence of hypertension in the group R3 was significantly lower than that in group R1,while the incidence of respiratory depression and tachycardia was significantly higher than that in group R1,the difference was statistically significant(P<0.05),RSS score and satisfaction scores in group R3 were significantly higher than those in group R1,the reaction score in group R3 was significantly lower than the group R1,the difference was statistically significant(P<0.05).Within group comparison,the mean arterial pressure and heart rate and respiratory rate at T2 and T3 in group R1 was significantly higher than those at T1,heart rate was significantly faster than T1,the respiratory rate was significantly faster than T1,the difference was statistically significant(P<0.05),T2 and T3 in group R3 were significantly slower than those at T0,the difference was statistically significant(P<0.05).Conclusion Remifentanil combined with dexmedetomidine can be safely and effectively used for awake intubation under glidescope guiding in difficult airway patients.In the full airway surface anesthesia,dexmedetomidine micropump 0.6μg/kg simultaneous target transfusion effect of the concentration of remifentanil 2.3ng/mL is a more reasonable medication.

AIM: To investigate effect of atrial natriuretic peptide (ANP) on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rat. METHODS: Mean arterial blood pressure (MAP) was recorded with model 6280 physiology intelligentialize grapher, nitric oxide (NO) and endothelin (ET) concentrations in plasma were measured after lipopolysaccharide (LPS) or following LPS ,ANP was injected into vein in rats. After experiment,lung water as well as pulmonary histopathological changes was measured and observed, respectively. RESULTS: Administration of LPS elicited a persistence decrease in MAP (8.1 kPa?2.6 kPa,at 4 h,P0.05); The histopathological of lung displayed markedly improved. CONCLUSION: ANP attenuates ALI induced by LPS in the rat. The effect of ANP may be via decreasing secretion of ET,NO and regulation arterial blood pressure. [

AIM: Niflumic acid (NFA) is known as a kind of inhibitor of calcium-activated chloride channel. The inhibition and mechanism of NFA on the proliferation of airway smooth muscle cells (ASMCs) were investigated. METHODS: Using [ 3H]-TdR incorporation method, we examined the effect of NFA (at concentration of 10 and 50 ?mol/L) on the proliferation of primarily ASMCs from BALB/c mouse. With confocal laser scanning microscope the [Ca 2+ ]i in ASMCs exposed to histamine was observed, and the opposed effects of NFA and nifedipine on histamine were also checked. Finally the effect of NFA on expression of MAPK in ASMCs was examined by indirect immunofluorescent assay. RESULTS: Compared with control group, the proliferation of NFA group was reduced markedly with dependent concentration. Histamine significantly improved the [Ca 2+ ]i in ASMCs, but NFA and nifedipine showed the inhibition on the effect of histamine. NFA reduced the level of MAPK expression in ASMCs. CONCLUSION: It is demonstrated that NFA inhibits the proliferation of ASMCs by reducing [Ca 2+ ]i and the expression level of MAPK. [

AIM: To observe the preventive effect of DNA vaccine based on human calcium-activated chloride channel 1 (hCLCA1) on airway hyperresponsiveness in asthmatic mice.METHODS: The DNA vaccine was constructed by inserting the hCLCA1 gene into pSecTag-2A, and then BALB/c mice were vaccinated by im. once every two weeks. Serum antibody was checked with the antigen of mCLCA3 by ELISA analysis. Asthma was induced with ovalbumin in the vaccinated mice. The airway pressure time index (APTI), the contractile responsiveness of isolated tracheal rings and the number of eosinophil in bronchoalveolar lavage (BAL) were investigated. Mice injected with pSecTag-2A, saline or normal mice were regarded as control groups. RESULTS: The title of antiserum binding to mCLCA3 in vaccine group was 1∶800 to 1∶(1 000) after three times vaccination. Compared with normal group, APTI, contractile responsiveness and number of eosinophil in vaccine group, pSecTag-2A or saline group were increased markedly (P

AIM: To investigate the relationship between inflammatory cell infiltration and proto-oncogenes expression in asthma. METHODS: Guinea pigs were used as asthma models challenged by ovoglobulin. Dot-blot, Northern-blot and immunochemical techniques were used to detect the expression of c-fos, c-myc, c-jun and c-sis. Inflammatory cell infiltration was showed by pathologic study.RESULTS: c-fos and c-myc mRNA could not be detected or expressed at very low level in control group. Those were greatly increased after the animals are challenged by ovoglobulin. Immunochemical study showed that Fos, Myc, Jun and Sis expressed at low level in control group, and those were increased after the challenge. There was little inflammatory cell infiltration in control group. Lymphocyte, neutrophil and eosinophil were detected immediately after the challenge, a great number of inflammation cells could be seen after 12-24 h of the challenge. Majority of neutrophil and eosinophil were under mucosa or in epithelium in airway. CONCLUSION: Oncogenes expression had strong relationship with airway inflammation.

AIM: To investigate the effects of fluvastatin on the airway remodeling in a guinea pig model of asthma. METHODS: Asthmatic guinea pig model was established by intraabdominal injection of ovalbumin and aluminium hydroxide and challenged with ovalbumin once every other day for 60 days. 30 guinea pigs were randomly divided into three groups: control group ( n= 10), asthma group ( n= 10) and fluvastatin plus asthma group ( n= 10) in which fluvastatin was inhaled at concentration of 0.5 g/L 30 min before every challenging. The thickness of airway smooth muscle layers of every three groups were compared after Haematin-Eosin staining by image analysis system. The level of ras mRNA in airway were examined by Dot-blot molecular hybridization. The expression levels of ras p21 were also examined by immunohistochemical technique. RESULTS: The mean thickness of airway smooth muscle in asthma group was (74 27?3 30) micrometer, greater than that of control group [(38 57?3 37) micrometer ( P

Objective To observe the effect of ulinastatin on tumor necrosis factor(TNF-α)and interleukin-6(IL-6)in radiation-induced lung injury.Methods Severity-two female SD rats were randomly divided into 3 groups as control group,irradiation group and treatment group(administered with Ulinastatin).Rats in irradiation group and treatment group were irradiated with linear accelerator at a single dose of 25 Gy.After irradiation rats in treatment group were injected daily with ulinastatin at a dose of 100000 U-kg-1·d-1 for 7 days through caudal vein while rats in control group and irradiation group were injected with the same volume of saline.Rats were killed at 2 h,4,8 and 24 weeks.Samples of lung tissues were observed by using HE staining.Expression of TNF-α in lung was determined by Western blot and expression of IL-6 in serum was determined by ELISA.Data were analyzed by SPSS software.Results Expressions of TNF-α in lung and IL-6 in serum increased significantly after irradiated in irradiation group compared with control group,and it reached the peak at 4 weeks(q=5.63、6.21,P＜0.01).Though expressions of TNF-α and IL-6 in ffeatment group also increased compared with control group,the difference between irradiation group and treatment group was statistic significantly(q=4.97、7.42,P＜0.01).Conclusions TNF-α and IL-6 play an important role in radiation-induced lung injury.Ulinastatin could suppress the inflammatory response and radiation-induced lung injury effectively by decreasing the levels of TNF-α and IL-6.