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慢性阻塞性肺疾病研究进展PPT课件.ppt 101页

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COPD patients suffer from reduced expiratory flow. As a result, the lungs may not fully empty before the next breath begins. This is particularly likely if the patient has to breathe faster as a result of physical activity.1 Because the lungs do not fully empty, they become progressively over inflated with each breath. This process is known as air trapping, which leads to hyperinflation.1 Air trapping reduces the ability of the patient to breathe in, which causes the sensation of breathlessness that typifies the disease. O'Donnell DE, Webb K. The etiology of dyspnea during exercise in COPD. Pulmonary and Critical Care Update 14, Lesson 15./downloads/education/online/Vol14_13_18.pdf. Accessed 24 February 2004. * * Inflammatory cells involved in COPD. Cigarette smoke activates macrophages and epithelial cells to release chemotactic factors that recruit neutrophils, monocytes and CD8+ T-lymphocytes from the circulation. They also release factors that activate fibroblasts leading to small airway obstruction (obstructive bronchiolitis). Proteases released from neutrophils and macrophages may cause mucus hypersecretion and emphysema. * In this study by Hogg et al, the small airways from 159 patients with sugically resected iung tissue was assessed. Subjects were from patients who required surgical treatment of small peripheral lung tumours and patients enrolled in the National Emphysema Treatment Trial (NETT). 39 patients had stage 0 (at risk), 39 stage 1, 22 stage 2, 16 stage 3 and 43 patients had stage 4 COPD according to the GOLD classification. The data showed that progression of COPD was strongly associated with an increase in the volume of tissue in the wall (p<0.001) and the accumulation of inflammatory mucous exudates in the lumen (p<0.001) of the airways. In addition, the percentage of airways containing polymorphonuclear neutrophils (p<0.001), macrophages (p<0.001), CD4+ cells (p=0.02) and CD8+ cells (p=0.038) increased as COPD progressed as did the absolute vo

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