【摘要 】 目的 观察慢性阻塞性肺疾病(COPD)合并肺心病尸检20例的肺部病变特征及其与肺构形重建的关系。方法 常规或低压(18.4～33.4mm Hg)福尔马林灌注固定肺组织。用点计数法检测大肺片的肺气肿百分值。常规切片、Zeiss显微测微器定量测量细支气管的病变特征和肺间质纤维化所占百分值。天狼猩红苦味酸染色，偏振光镜观察，真彩色图像分析Ⅰ、Ⅲ两型胶原分布比值。结果 COPD病例中以不规则型和囊泡型肺气肿最多见(17/20)，13例有中度和重度肺气肿，心重>400g者6例。肺纤维化组织占肺总切面积平均为(27.1±2.9)%,对照组为(12.0±1.8)%;Ⅰ型与Ⅲ型胶原面积比为5.6∶1,对照组为1.3∶1；COPD组1504支细支气管均有慢性细支气管炎，其中合并急性炎症者占38%;管腔狭窄和纤维性闭锁者占53%。结论 急、慢性细支气管炎和细支气管周围炎是COPD的重要肺部病变，也是导致肺组织和血管构形重建的重要环节。

    

Department of Pathology, Tongji Medical University, Wuhan 430030

【Abstract 】 Objective Tounderstand the pathological characteristics of the lungs in 20 autopsy cases of chronicobstructive pulmonary disease(COPD) complicated with cor pulmonale and its relationshipwith structural remodeling of the lungs. Methods The lungs of 20 autopsy cases of COPDcomplicated with cor pulmonale were fixed in 10% formalin or by low pressure 18.4～33.4mm Hg perfusion with 10% formalin. The lungs were cut sagitally into large slices with 2cm in thickness, and the percentage of the emphysematous areas was calculated by pointcounting. The pathological characteristics of bronchioles and the stromal fibrosis areawere examined microscopically and quantitatively using a latticed micrometer (Zeiss). Thedistribution and the ratio of type I to type Ⅲ collagen in the lung tissue weredetermined using a sirius red-polarizing microscopy-morphmetry method. ResultsOf the 20cases of COPD,irregular and saccular emphysema were the most frequent (17/20).10 cases hadmoderate and high degree of emphysema, and 6 cases showed hypertrophy of the rightventricle (heart weight >400 g). The mean area of stromal fibrosis auounted for totalarea of the examined lungs was (27.1±2.9)% and control group (12.0±1.8)%.The ratio ofthe area of the type Ⅰcollagen to type Ⅲ collagen was 5.6∶1 (control group 1.3∶1).All 1504 bronchioles showed chronic inflammation, 38% of which revealed acuteexacerbation, and 53% of which showed lumen stenosis and fibrotic obstruction. Conclusions Acuteand chronic bronchiolitis and peribronchiolitis are the essential pathological changes in COPD, and also are the key link of the structural remodeling of the pulmonary tissue andvessels.

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