Objective To establish animal model of acute lung injury induced by sulfur mustard (SM) in rats,in order to observe the histomorphologic change of lung,protein content and cell numbers in bronchoalveolar lavage fluid (BALF),and serum inflammatory factors reaction in different time phases.Methods 72 male rats were selected,then randomly divided into three groups:SM group (n =32),propylene glycol group (n =32),and control group (n =8).The rats in SM group were injected intratracheally diluted SM (2 mg/kg,0.1 ml),the rats in propylene glycol group were injected intratracheally propylene glycol 0.1 ml,and status quo was kept with the control group.BALF,serum,and lung tissue were obtained in 6h,24h,48h,and 72h respectively.HE and immunohistochemistry staining were used to observe histomorphologic change and inflammatory cell infiltration.The alveolar interval area,content of inflammatory factor in serum,total albumen and cell number in BALF were measured.Results SM group:①The epithelium cells of the damaged bronchioles were shed,and the focal ulcer formed.②Dilatating and congestive vessels were observed in pulmonary interstitial,and lymphocyte is the main element of the inflammatory infiltration.③Inflammatory exudate and inflammatory cells appeared in alveolar cavity,which the albumen content and cell number in BALF peaked in 48 hours.④The content of tumor necrosis factor-α,interleukin-1β,and interleukin-6 in serum peaked in 24 hours.⑤ The alveolar interval area widened obviously,and the damage degree was time dependent.Results in the propylene glycol group was the same with those in the control group.Conclusions SM (2 mg/kg) can induce histomorphologic change similar to acute respiratory distress syndrome.Lymphocyte is the main element of inflammatory infiltration.BALF and serum results suggest there was temporary inflammation,and the damage degree is time dependent.

Objective To establish the sulfur mustard (SM ) induced tracheal injury model in rat and to investigate its mecha-nism .Methods Male rats (SD) were anesthetized and intra-tracheally intubated .The SM group was intra-tracheally injected by 2 mg/kg of diluted SM ,while the propylene glycol control group only by 0 .1mL of propylene glycol and the normal control group had no any treatment .The tissue and blood samples were taken for conducting the HE and immunohistochemical staining and measuring serum enzymes and andinflammatory factors .Results In the SM group ,a large number of lymphocytes infiltration in submucosa were observed;the positive expression of caspase-3 and caspase-9 were observed in epithelium and submucosa ;serum levels of TNF-α,IL-1β,IL-6 reached the peak in 24 h;serum levels of LDH ,GP ,BARS reached the peak in 6h ,so did GGT in 24 h .In the propyl-ene glycol control group and the normal control group ,lymphocytes ,macrophages and neutrophils were rare in submucosa .Conclu-sion The mechanism of SM (2 mg/kg) induced acute tracheal injury involves the inflammatory reaction ,apoptosis and oxidative stress ,moreover the lesion degree has the correlation with time .

Objective To establish an animal model for rat respiratory tract injury due to sulfur mustard (SM),and observe the morphologic changes of tracheal tissues and epithelial cells in SM-induced injury.Methods Male SD rats (n =72)were randomly divided into three groups (SM group,propylene glycol group,and normal group).The rats in the SM (2 mg/kg)group were injected intratracheally with diluted SM (0.1 ml).Histomorphologic and cytomorphogic changes of the specimen were observed under light and electron microscopy.Results In the SM group,histomorphologic changes included shed tracheal epithelial cells,focal ulcer formation,deranged cilia,increased glands in the lamia propria mucosae,and inflammatory cells invading the submucosa.The cytomorphologic changes were as follows:the cellular membranes lacking,medullary changes in the mitochondria with difficult to discern mitochondrial cristae appeared in goblet cells,and difficult to discern karyotheca,karyopyknosis,and margination of the nuclear chromatin in cilia,basal cells,fibroblasts.The structure of tracheal tissue and epithelial cells of the propylene glycol group was the same as the control group.Conclusions SM (2 mg/kg)can cause acute injury of tissues and multi-epithelial cells of the rat trachea.The degree of injury is positively correlated to the duration of time.SM mainly affects the cellular membranes and organelles of goblet cells,as well as nuclear chromatin of cilia,basal cells,and fibroblasts.

目的:观察高流体静力压对大隐静脉和脾静脉管壁滋养血管的影响.方法:收集曲张大隐静脉和高压性脾静脉标本(疾病组),以及正常大隐静脉和脾静脉标本(正常对照组).采用CD34免疫组化染色与Masson染色,计算各组管壁滋养血管的数量和平均截面积,并定量分析.结果:形态学观察显示,两个疾病组管壁滋养血管均较各自的对照组明显增生.定量分析显示,两个疾病组的滋养血管数量、平均截面积在中膜或外膜,均明显大于各自的正常对照组(均P＜0.05);脾静脉外膜滋养血管数量疾病组与其正常对照组差值明显大于大隐静脉,大隐静脉外膜滋养血管疾病组与其正常对照组平均截面积差值明显大于脾静脉(均P＜0.05),但两种血管间以上差值在中膜中的差异均无统计学意义(均P＞0.05).结论:高流体静力压下大隐静脉和脾静脉管壁滋养血管明显增生,两者变化存在异质性,大隐静脉中以管径增大为主,脾静脉中以数量增多为主.

近年来,随着我国大气污染的加重,支气管哮喘(简称哮喘)的发病率逐年上升。哮喘目前还不能完全根治,反复发作为其特点,故及早诊断和规范化治疗至关重要。气道慢性炎症是哮喘的本质,其主要病理生理特征是气道高反应性[1]。因此,准确地判断气道炎症程度,有助于提高患者的治疗依从性。呼出气一氧化氮( fractional exhaled nitric oxide, Fe-NO)是反映气道炎症的指标之一,可与支气管激发试验和呼出气冷凝液pH值检测互补,现已广泛应用于临床[2]。为此,2005年美国胸科学会、欧洲呼吸学会已将FeNO推荐为哮喘气道炎症监测指标。本文重点就FeNO与哮喘诊治的关系概述如下。

Cough variant asthma（CVA） is a special typologic bronchial asthma （asthma） which presents solely with chronic cough. CVA is a form of asthma,CVA shares a number of pathophysiological features with classic asthma. More importantly, 30% to 40% of adult patients with CVA, unless adequately treated, may progress to classic asthma. Cellular infiltration and airway remodeling are pathological basis of CVA. CVA may call an insidious asthma,it was neglected freguently by clinician, and the patients were missed correct diagnosis and treatment. To know correctly pathophysiological features of CVA,it is important significance for clinical treatment,and may decrease incidence of asthma. In this review,we analyzed the correlation between CVA and inflammatory reaction,airway remodeling. Key words: Cough variant asthma Asthma Cellular infiltration Airway remodeling

Objective To establish rat model of pulmonary injury induced by sulfur mustard (SM) to investigate the apoptosis and oxidative stress in the injured lung.Methods 72 male rats were selected,then randomly divided into SM group (n =32),propylene glycol group (n =32),and normal control group (n =8).The rats in SM group were injected intratracheally diluted SM (2 mg/kg,0.1 ml),the rats in propylene glycol group were injected intratracheally propylene glycol 0.1 ml,meanwhile the status quo was kept with the normal control group.Then the SM-induced apoptosis and oxidative stress were observed by electron microscope,immunohistochemical staining,and bronchoalveolar lavage fluid (BALF) examination.Results SM group:①The content of lactate dehydrogenase and glutathione peroxidase in BALF peaked in 6h.②There was local defect of cellular membrane in alveolar epithelial type Ⅰ cells,while microvilli missed as well as disarranged in alveolar epithelial type Ⅱ cells.The appearance of ribosome detached from rough endoplasmic reticulum,and illegibility of mitochondrial cristae were observed in both types of cells.③Apoptosis was observed significantly increasing in the alveolar septum.Results in the propylene glycol group was the same with those in the normal control group.Conclusions Apoptosis and oxidative stress are two main mechanism characteristics of SM (2 mg/kg) induced pulmonary injury in rats.