Objective To observe the expression of angiotensin-converting enzyme( ACE) and ACE2 in rat lung and kidney at different time point after smoke inhalation injury and to explore the possible mechanism. Methods Thirty healthy male SD rats were randomly divided into five groups( n = 6 in each group) , ie. a normal control group, and 4 injury groups of 1 h, 4 h, 10 h and 24 h respectively after 30 min of dense smoke inhalation. The rats were sacrificed at different time point. Lung and kidney tissue samples were collected for measurement of lung wet/dry weight ratio( W/D) , pathological study by HE staining, and ACE and ACE2 expression by immunochemistry staining. Results The inhaled rats all displayed acute lung injury symptoms. The lung W/D in the injury groups were significantly higher compared to the normal control group ( P lt; 0. 05, P lt; 0. 01) . ACE and ACE2 were expressed on cellular membrane of normal lung and kidney. The expression of ACE in lung was increased immediately after injury and the expression of ACE2 in lung was increased at 4 h after injury. No significant changes of the expression of ACE and ACE2 in kidney were observed in the five groups. Conclusion The imbalances of expression of ACE and ACE2 in lung might play an important role in the pathogenesis of smoke inhalation injury.
Objective To investigate the protective effects of ulinastatin on acute lung injury ( ALI)induced by seawater drowning in rats. Methods Thirty male SD rats were randomly divided into three groups, ie. a control group, a model group, and an ulinastatin treatment group. The rats in the model group and the ulinastatin treatment group received intratracheal artificial seawater ( 4 mL/kg) instillation. Then the ulinastatin treatment group received ulinastatin ( 100 000 U/kg) injection after infusion of seawater while the model group received an injection of same amount of saline. The rats were sacrificed at 4 hours after instillation. The pathological changes of lung were evaluated by hematoxylin-eosin stain under light microscope. Lung wet/dry weight ratios were measured to assess the level of pulmonary edema.Concentrations of tumor necrosis factor ( TNF) -α, interleukin ( IL) -1β, IL-6, and IL-10 in bronchoalveolar lavage fluid ( BALF) were detected by enzyme-linked immunosorbent assay ( ELISA) . The myeloperoxidase activity in lung tissue homogenates were measured by colorimetric method. Results Ulinastatin treatmentsignificantly relieved the decline of PaO2 and lung pathological changes, inhibited myeloperoxidase activity,and reduced lung wet/dry weight ratios. Ulinastatin also inhibited the release of TNF-α, IL-1β, and IL-6,whereas increased the expression of IL-10 simultaneously. Conclusion Ulinastatin attenuates seawater induced ALI, which may be related to its inhibitory effects on inflammation reaction through regulating cytokine secretion.
ObjectiveTo evaluate the safety and efficacy of non-invasive positive pressure ventilation (NIPPV) combined with fiberoptic bronchoscopy(FB) on acute exacerbation of chronic obstructive puhmonary disease (AECOPD) patients with acute respiratory failure. MethodsA prospective study was conducted on the AECOPD patients with respiratory failure in respiratory intensive care unit of Tangdu Hospital of Fourth Military Medicine University from February 2010 to February 2011.They were randomly divided into a case group and a control group.The case group was administrated FB and lavage after one hour of NIPPV treatment.The control group was administrated NIPPV without FB and lavage.Other treatment regimen was the same in two groups. ResultsThere were 51 subjects recruited in the study, 25 subjects in the case group and 26 subjects in the control group.All variables at baseline were matched (P > 0.05).All variables improved after one hour of NIPPV before FB, without significant difference between two groups (P > 0.05).During the period of FB, heart rate in the case group was faster than that in the control group (P < 0.05), and other variables were not significantly different between two groups (P > 0.05).Both groups received NIPPV for one hour after FB, the variables including heart rate, respiratory rate, pH, PaO2, PaCO2 were statistically significant between two groups(P < 0.05).At the time of 24 hours after FB, the variables including mean arterial pressure, heart rate, respiratory rate, pH, PaO2 and PaCO2 in the case group were nearly recovered, and differences between two groups were significant (P < 0.05).The positive rate of sputum culture was significantly higher in the case group than that in the control group[88.0%(22/25) vs.58.6%(14/26)].Success rate in the case group were obviously superior to that in control group.The cases of failure, death and refusing in the case group were lower than those in the control group.Complications in two groups had no significant difference (P > 0.05).There was not serious complication such as hear arrest, hemoptysis and apnea during the process of NIPPV combined with early FB. Conclusion It deserves to be used in clinic because of the safety, efficacy and feasible for most of AECOPD patients through NIPPV combined with early FB.
ObjectiveTo investigate the molecular pathogenesis of pulmonary fibrosis induced by bleomycin in a murine model,and provide novel insights for clinical diagnosis and treatment. MethodsFrom Gene Expression Omnibus,we downloaded microarray data extracted from experiments of bleomycin induced pulmonary fibrosis in wild-type mice. With BRB-Array Tools,differentially expressed genes at different time points during disease development were screened,selected and analyzed by DAVID software. ResultsBRB array analysis identified 45101 differentially expressed genes. After induction by bleomycin on 7th day,1164 genes and 735 genes were significantly up-regulated and down-regulated (P<0.05,fold change>2),respectively. On 14th day,731 genes and 390 genes were significantly up-regulated and down-regulated (P<0.05,fold change>2),respectively. DAVID analysis revealed that the up-regulated genes were significantly enriched in cell cycle,p53 signaling and chemokine signaling pathway,damaging reaction and collagen metabolism gene sets. While the down-regulated genes were enriched in the drug metabolism pathway gene set. ConclusionsBioinformatics methodologies are able to efficiently analyze microarray data and extract its underlying information,provide novel insights for major molecular events and shift of cell signaling pathway during pulmonary fibrosis progression,and furthermore,finding molecular markers for early diagnosis and therapeutic targets.
Objective To investigate whether sodium tanshinone ⅡA sulphonate ( STS) treatment attenuates pulmonary edema of seawater drowning ( PE-SWD) , and examine the effects of STS on Na-KATPase(NKA) in PE-SWD. Methods Thirty-six rats were randomly divided into there groups, ie. a normal group ( NG) , a seawater group ( SG) , and a STS treatment group ( TG) . The rat model of PE-SWD was established by seawater instillation. PaO2 , histological changes of lungs, lung wet /dry weight ratio ( W/D) ,pulmonary microvascular permeability ( PMVP) , and NKA activity were detected. Western blot were used to test the effects of STS on NKA-α1 expression. Results Seawater instillation decreased PaO2 and the expression of NKA, while increased W/D ratio and PMVP. At 2 h after seawater instillation, the PaO2 in the TG group were significantly higher than those in the SG group, and peaked at 4 h after seawater instillation.Histological examination showed that there were hemorrhage, edema, markedly thickened alveolar wall, and infiltration of inflammatory cells in alveolar spaces in the SG group, but lung injury was significantly alleviated in the TG group. W/D ratio and PMVP in the TG group were significantly lower than those in the SG group. Additionally, NKA activity and NKA-α1 expression were significantly higher in the TG group than those in the SG group. Conclusion STS treatment can attenuate pulmonary edema of seawater drowning which may be related with up-regulating Na-K-ATPase activity and expression.