烟草烟雾诱导的慢性阻塞性肺疾病模型大鼠消化道的病理特点

目的观察慢性阻塞性肺疾病(COPD)模型大鼠消化道的病理改变,为探究COPD营养不良的机制提供理论依据。方法采用单纯烟草烟雾暴露的方法建立COPD大鼠模型。造模结束后,检查大鼠肺功能、动脉血气、支气管肺泡灌洗液炎症细胞和炎症介质水平以及肺组织、肝、脾、胃、小肠的病理变化。结果与正常对照组大鼠相比,模型组大鼠体质量明显减轻;功能残气量、肺总量上升,静态肺顺应性增加,呼气流速50毫秒用力呼气量/用力肺活量比值下降;肺泡结构大小不一、部分肺泡间隔断裂、融合;支气管肺泡灌洗液中,炎症细胞总数及分类计数(中性粒细胞、巨噬细胞及淋巴细胞)均高于对照组,促炎介质白细胞介素-6(IL-6)和单核细胞趋化蛋白1水平高于对照组,而抗炎介质IL-10低于对照组;肝小叶中央静脉充血伴炎症细胞浸润,肝细胞轻度水肿、脾出现淤血、胃出现轻度糜烂、小肠黏膜萎缩伴炎症细胞浸润。结论在COPD大鼠模型中,肝、脾、胃黏膜、小肠黏膜等消化道组织均出现充血、水肿、淤血、糜烂、炎症细胞浸润等炎症性病理改变,这些病变可能与COPD营养不良有关。

Pathological characteristics of digestive tract in rats with chronic obstructive pulmonary disease induced by tobacco smoke

Objective To observe the pathological changes of the digestive tract of rats with chronic obstructive pulmonary disease(COPD),as well as to provide a theoretical basis for exploring the mechanism of COPD dystrophy.Methods The COPD rat model was established by cigarette smoke(CS)exposure.Lung functions were measured using Buxco lung function measurement system.Arterial blood gas parameters were examined with GEM3000 blood gas analyzer.The inflammatory cells were counted and the level of interlukin-6(IL-6),monocyte chemo-attractant protein-1(MCP-1)and IL-10 in bronchoalveolar lavage fluid(BALF)were assayed with enzyme-linked immunosorbent assay.Pathological changes of lung tissue,liver,spleen,stomach,small intestine were observed.Results At the end of modeling,the weight of the model group rats were significantly lower than those of the control group.Compared with control rats,the CS exposed rats presented typical COPD-like lung function decline indicated by increases in functional residual volume(FRC),total lung capacity(TLC),Chord compliance(Cchord),as well as a decrease in the FEV50/FVC ratio.Damaged alveolar walls and pulmonary bullae were observed in rats′lungs exposed to CS.In alveolar lavage fluid,the total number of inflammatory cells and the categorical counts(neutrophils,macrophages,and lymphocytes)were higher than those of the control group,as well as the levels of IL-6 and MCP-1 as proinflammatory mediators.The anti-inflammatory cytokine IL-10 was lower than that of the control group.Moreover,the histological staining showed that a little congestion in the central hepatic lobule with inflammatory cell infiltration and mild hepatic edema,a small amount of congestion in the spleen,mild erosion in the stomach,small intestine mucosal atrophy with a small amount of inflammatory cell infiltration.Conclusions In COPD,gastrointestinal pathological changes including hyperemia,edema,congestion,erosion,and inflammatory cell infiltration are observed in the digestive tract tissues including liver,spleen,gastric mucosa,and small intestinal mucosa.