探讨先天性支气管囊肿的临床、影像学特点及治疗方法。方法:对19例经手术和病理活检证实的先天性支气管囊肿患者的临床资料进行了回顾性分析。结果:本组19例患者中,肺内囊肿15例(79%),纵隔囊肿4例。临床症状表现为咳嗽14例(74%),咯血7例,呼吸困难5例,胸痛5例;其中13例患者(68%)出现并发症,包括感染、大咯血、气胸和胸膜炎等。影像学表现为单发边界清楚的软组织或水样密度包块影4例,单发薄壁含气囊腔4例,单发圆形含气液平的包块影7例,多发环形透光影4例。所有患者均进行了开胸囊肿切除术。结论:先天性支气管囊肿多位于肺内,常见临床症状为咳嗽,影像学以单发含气液平的包块影为多见,手术切除是最好的治疗方法。
Objective To investigate the role of macrophage stimulating protein (MSP) in the pathogenesis of chronic obstructive pulmonary disease (COPD). Methods Ninety subjects were recruited from health examination center, outpatient or inpatient department in Affiliated Hospital of North Sichuan Medical College from July 2013 to December 2013. They were divided intoahealthy control group, a stable COPD group, and an acute exacerbation of COPD (AECOPD) group with 30 subjects in each group. The levels of MSP, interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α (TNF-α) in the plasma of all subjects, as well as the levels of MSP in the induced sputum of the AECOPD and the stable COPD patients were assessed by enzyme-linked-immuno-sorbent assay. Results The concentrations of MSP, IL-6, IL-8 and TNF-α in the plasma of the patients with COPD were obviously higher than those of the healthy controls (P<0.05) while much higher in AECOPD patients than those in stable COPD patients (P<0.01).The concentration of MSP in the induced sputum of the patients with AECOPD was higher than that in the stable COPD patients (P<0.01). The concentrations of MSP in the serum and induced sputum as well as serum levels of IL-6, IL-8 and TNF-α in the patients with COPD were negatively correlated with the level of FEV1%pred. The concentrations of MSP in the serum and induced sputum in the COPD patients were positively correlated with the concentrations of IL-6, IL-8 and TNF-α. Conclusions The concentrations of serum and induced sputum MSP, and the serum concentrations of IL-6, IL-8 and TNF-α in COPD patients are related to the severity of the disease. MSP may play an important role in the pathogenesis of COPD. The mechanism might be mainly involved in the regulation of airway inflammation.
ObjectiveTo investigate the role and mechanism of S100A8/A9 in rat model of chronic obstructive pulmonary disease (COPD). Methods Twelve Wistar rats were randomly divided into a normal control group and a COPD group. The COPD model was established by exposing the rats to cigarette smoke and injected lipopolysaccharide (LPS) in bronchus for 1 month. The pathological changes of the lung tissue were observed under light microscope, and the emphysema indexes of pulmonary mean linear intercept (MLI), mean alveolar numbers (MAN) and pulmonary alveolar area (PAA) were analyzed by image analysis system. The concentrations of S100A8/A9 in serum and bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay. The mRNA expression levels of S100A8, S100A9, Toll-like receptor-4 (TLR4) and myeloid differentiation factor 88 (MyD88) of lung tissues were measured by real time polymerase chain reaction. The protein expressions of S100A8/A9, TLR4 and MyD88 of lung tissues were detected by immunohistochemistry. Results After cigarette smoking and LPS injection for 1 month, the rat lung tissue appeared in accordance with the typical pathological changes of COPD. The MLI, MAN and PAA had obvious difference compared with the normal control group (P<0.05). The concentrations of S100A8/A9 protein in BALF and serum of the COPD group were obviously higher than those of the normal control group (P<0.05). The levels of S100A8, S100A9, TLR4 and MyD88 mRNA of lung tissues in the COPD group were obviously higher than those in the normal control group (P<0.05), and the expression levels of S100A8 and S100A9 mRNA were positively correlated with the expression levels of TLR4 and MyD88 mRNA respectively (P<0.05). The levels of S100A8/A9, TLR4 and MyD88 protein of lung tissues in COPD group were obviously higher than those in normal control group (P<0.05), and the levels of S100A8/A9 protein were positively correlated with the levels of MyD88 and TLR4 protein (P<0.05). Conclusions As a new inflammatory mediator, S100A8/A9 may be involved in the occurrence and development of COPD. By up-regulating the expression of TLR4 and MyD88, the classical TLR4-MyD88 inflammatory pathway is activated, thus promotes the occurrence and development of COPD.
Objective To investigate the preventive effect of simvastatin，a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor，on hypoxic pulmonary hypertension and the relation between it and the angiotensin Ⅱ receptor-1（AT1R） expression in pulmonary arteriole.Methods Thirty male Sprague-Drawley rats were randomly allocated into three groups：a control group，a hypoxic group and a simvastatin preventive group.The animal model of hypoxic pulmonary hypertension was established by exposing the rats to normobaric hypoxic condition（8 h×6 d×3 w），and the preventive group were treated with simvastatin 10 mg/kg before hypoxic processing while the control and hypoxic groups were treated with sodium chloride.The mean pulmonary pressure（mPAP），serum cholesterol concentration，right ventricular hypertrophy index [RV/（LV+S）]，percentage of the wall thickness in the external diameter（WT%），percentage of the wall area in the total vascular area（WA%），and the AT1R expression in pulmonary arterioles were measured.Results When compared with the hypoxic group，in the preventive group，the mPAP and RV/（LV+S）obviously reduced [（22.6±3.86）mm Hg vs （29.3±2.27）mm Hg，（25.13±0.75）% vs （33.18±1.58）%，Plt;0.01 respectively]，the indices of wall thickness of rat pulmonary arteriole and area also decreased significantly [WT%：（15.98±1.96）% vs （25.14±1.85）%；WA%：（54.60±3.94）% vs 74.77±4.52）%；Plt;0.01 respectively]，and the positive degree of AT1R still lessened noticeably（1.23±0.09 vs 1.57±0.13，Plt;0.01）.All of the indices above in the hypoxic group increased markedly compared with the control group（Plt;0.01 respectively）.However，the differences of serum cholesterol among three groups were not significant（Pgt;0.05）.Conclusions Simvastatin can suppress the expression of AT1R in pulmonary vessel and prevent hypoxic pulmonary hypertension.
ObjectiveTo compare the difference of respiratory mechanics parameters between three different spontaneous breathing trials on COPD patients in weaning process. Methods17 patients with COPD underwent mechanical ventilation for at least 48 hours who were stable and ready for weaning were enrolled. All patients underwent three spontaneous breathing trials, ie, automatic tube compensation (ATC,compensation level 100%),low level pressure support ventilation (PSV,7 cm H2O) and T-piece. Each spontaneous breathing trials continued for 10 minutes. Before each autonomous respiration experiment ended,the respiratory mechanics parameters including high airway pressure (PIP),breathing rate (RR),blood oxygen saturation (SaO2),airway occlusion pressure at 0.1 second (P0.1),maximal inspiratory mouth pressure(Pimax) and rapid shallow breathing index (RSBI) were measured. Their differences between three spontaneous breathing trials were compared. Results12 patients successfully completed three different methods of spontaneous breathing test. Compared with the T-piece,P0.1,Pimax,RSBI and RR in the COPD patients using low level PSV and ATC were significantly decreased while VT and SaO2 were increased. The difference of each parameter in the low level PSV group and the ATC group had statistical significance compared with T-piece group (P<0.05). Compared with the low PSV group,P0.1,Pimax,RSBI and RR in ATC group were elevated while PIP,VT and SaO2 were reduced. The differences of P0.1,Pimax,RSBI,PIP and RR between two groups were statistically significant (P<0.05). ConclusionFor COPD patients in weaning process with spontaneous breathing trial,both low levels of PSV and ATC are better than T-piece,and the patients are more comfortable with ATC100% than PSV.
ObjectiveTo investigate the effect of maresin-1 (MaR1) on lung inflammation and MAPK signaling pathway in asthmatic mice.MethodsTwenty-four female BALB/c mice were randomly divided into normal group, asthma model group, MaR1 group and dexamethasone group. The asthma model was successfully established by using ovalbumin (OVA) combined with aluminum hydroxide, and then MaR1 and dexamethasone were respectively given to asthmatic mice. Serum, bronchoalveolar lavage fluid (BALF) and lung tissue were collected for further analysis. Pathological changes of lung tissue in mice were detected by hematoxylin-eosin and periodic acid-Schiff. Proportion of inflammatory cells in BALF classified by Swiss-Giemsa staining. Th2-related inflammatory cytokines, interleukin (IL)-4, IL-5, IL-13 and IgE in serum and BALF were detected by enzyme linked immunosorbent assay. The protein concentration of p-p38 and p-JNK in lung tissues were detected by Western blot.ResultsCompared with the normal group, the asthma model group had increased both airway inflammation and the number of goblet cells significantly (P<0.05). The number of various inflammatory cells in BALF had also increased significantly (P<0.05). The levels of IL-4, IL-5 and IL-13 in BALF and IgE and OVA-specific-IgE in serum were significantly increased (P<0.05). The protein contents of p-p38 and p-JNK in lung tissues were significantly increased (P<0.05). Compared with the asthma model group, both MaR1 and dexamethasone group had reduced inflammation and mucus secretion in lung tissue, number of inflammatory cells in BALF (P<0.05), levels of related inflammatory cytokines in BALF and IgE in serum (P<0.05), and expression of p-p38 and p-JNK proteins in lung tissue (P<0.05).ConclusionsMaR1 can inhibit the production and release of both Th2-related inflammatory cytokines and IgE, effectively reduce the inflammatory response and mucus production in lung tissues of asthmatic mice, with similar effect to dexamethasone. The mechanism may be related to the down-regulation of MAPKs signaling pathway.
Objective To observe the expression of S100A8 and S100A9 in alveolar macrophages (AMs) of chronic obstructive pulmonary disease (COPD) rats, and explore the effect on the release of inflammatory mediators from AMs in COPD rats. Methods Twelve adult male Wistar rats were randomly divided into a normal control group and a COPD group. The COPD model was established by exposing the rats to cigarette smoke and intratracheal injection of endotoxin for 1 month. The pathological changes of lung tissue of rats were observed under light microscope. Total cells counts and the number of AMs, lymphocytes, neutrophils in bronchoalveolar lavage fluid (BALF) of two groups were examined by Wright's staining methods. Rat AMs from the control group and the COPD group were isolated and cultured, and then treated with different doses of S100A8 and S100A9 for 6 hours and 12 hours. The levels of interleukin (IL)-8, IL-6 and tumour necrosis factor-α (TNF-α) in the AMs supernatants were measured by enzyme linked immunosorbent assay. The expression of S100A8 and S100A9 mRNA in AMs of rats were observed by in situ hybridization. The immunohistochemical method was used to observed the expression of S100A8/A9 protein of AMs. Results After cigarette smoking combined with intratracheal injection of endotoxin for 1 month, the lung tissue of rats showed typical pathological changes of COPD. Total cell counts and the number of AMs, lymphocytes, neutrophils in BALF of the COPD rats were significantly higher than those of the normal rats (P<0.05). Among them, the increase in the number of AMs was the most obvious. Compared with the control group, the expression of S100A8 mRNA, S100A9 mRNA and S100A8/A9 protein in AMs of the COPD group were up-regulated significantly (P<0.05). After the AMs of COPD rats were treated with S100A8 and S100A9, the contents of IL-8, IL-6 and TNF-α in AMs supernatants increased significantly in a time- and dose-dependent manner. When the AMs were treated with the same dose of S100A8 and S100A9 for the same time, the levels of IL-8, IL-6 and TNF-α in the AMs supernatant of the COPD group were higher than those of the normal control group. Conclusions The expression of S100A8 and S100A9 in cultured COPD rat AMs is significantly increased. S100A8 and S100A9 can promote the secretion and release of inflammatory factors IL-6, IL-8 and TNF-α from AMs of COPD rats in a time and dose-dependent manner. The effects of S100A8 and S100A9 on the secretion of IL-6, IL-8 and TNF-α in AM of COPD rats are significantly enhanced compared with those of normal rats.