摘要:目的 研究肺功能正常吸烟者和慢性阻塞性肺疾病(COPD)患者肺腺泡动脉炎症的病理特点。方法 取手术切除的远离周围型肺癌的正常肺组织,分肺功能正常不吸烟组(A组,10例)、肺功能正常吸烟组(B组,13例)、吸烟COPD稳定期组(C组,10例),比较3组肺腺泡动脉病理结构改变、炎性细胞在非肌型动脉(NMA)、部分肌型动脉(PMA)外膜,肌型动脉(MA)内、中、外膜的浸润水平,并分析其与临床指标的相关性。结果 (1)B组(32.7±7.7)、C组(37.4±4.5)较A组(24.4±5.0)MA比例增高,MA内、中膜增厚,C组MA外膜胶原纤维增生,面积明显增大。(2)B组和C组CD+45白细胞、CD3+总T淋巴细胞、CD8+T淋巴细胞在各型肺腺泡动脉表达的范围和程度均较A组增高,以CD8+T淋巴细胞增高为主,炎性细胞浸润以肺腺泡NMA最为明显,在MA以外膜最显著,且C组较B组明显;而CD4+T淋巴细胞、B淋巴细胞、巨噬细胞、中性粒细胞在3组各型肺腺泡动脉浸润程度比较差异均无统计学意义(P值均>0.05)。(3)CD45+白细胞、CD3+总T淋巴细胞、CD8+T 淋巴细胞在MA的浸润程度与MA管壁厚度、吸烟指数呈正相关,与第1秒用力呼气容积占预计值百分比呈负相关,CD3+总T淋巴细胞、CD8+T淋巴细胞浸润程度与BODE指数呈正相关,CD8+T淋巴细胞浸润程度与6 min步行距离呈负相关。结论 肺功能正常吸烟者和COPD患者均已出现以CD8+T 淋巴细胞浸润为特征的同性质炎症反应,炎症累及各型肺腺泡动脉,肺动脉炎症是影响COPD临床病程发展的重要因素之一。%Objective To study the pathological characteristics of intra-acinar pulmonary artery inflammation and its correlation with smoking index and disease progression in smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD).Methods Patients requiting lung resection for peripheral lung cancer were divided into group A (nonsmokers with normal lung function,n = 10), group B (smokers with normal lung function, n = 13), and group C (smokers with stable COPD,n = 10).The lung tissue far away from rumor were resected to compare the pathological changes of intraacinar pulmonary arteries and infiltration level of inflammatory cell in pulmonary non-muscularized arteries (NMA), pulmonary partially muscularized arteries (PMA) and muscularized arteries (MA) among the three groups.The correlation analysis was made among infiltration level, smoking index, percentage of predicted value of forced expiratory volume in one second (FEV,% Pred), six-minute-walk distance (6MWD) and BODE index.Results (1) Both group B and group C showed the intima and media thickness of MA was significantly higher, the lumen area of MA was narrower and the proportion of MA was higher, and collagenous fiber of MA adventitial proliferated and area increased in group C(P <0.05 or P <0.01).(2) In group B and group C, the percentage of the intra-acinar pulmonary arteries that contained leukocytes, T lymphocytes, CD8+ T lymphocytes and the number of these positive cells infiltrating the intraacinar pulmonary arteries were increased, especially an increased number of CD8+ T lymphocytes infiltrating in the arterial adventitia as compared with group A, moreover there were significant difference between group C and group B (P < 0.05 or P < 0.01).In group B and group C, the degree of these positive cellsinfiltrating NMA, PMA and MA presented a decreasing sequence (P < 0.05 or P < 0.01).Among the intima, media and adventitia of MA, the infiltration of these positive cells was the highest in the adventitia.Among group A, group B and group C, infiltration degree of CD4+ T lymphocyte, B lymphocyte, macrophage and neutrophil demonstrated no significant difference, also among NMA, PMA and MA (P > 0.05).(3)The number of leukocytes, T lymphocytes, CD8+T lymphocytes infiltrating MA showed a positive correlation with the thickness of MA (r =0.563,0.627,0.589 ,P <0.01 ,respectively) and smoking index (r =0.551,0.665, 0.600, P < 0.01, respectively), moreover the degree of these cells infiltrating MA demonstrated negative correlation with FEV1 % Pred (r = - 0.763, - 0.703, - 0.767, P < 0.01, respectively).Also infiltrating degree of T lymphocytes and CD8+ T lymphocytes was positively correlated with BODE(r = 0.390,0.476,P < 0.05, respectively). Furthermore the infiltrating degree of CD8+ T lymphocytes had negative correlation with 6MWD (r = - 0.356, P < 0.05).Conclusions (1) Pulmonary arterial inflammation appears in smokers with normal lung function and smokers with COPD patients.It involves in all types of intra-acinar pulmonary arteries especially NMA and infiltrates whole layer of MA with a characteristic of CDs+T lymphocytes infiltrating in the adventitia of intra-acinar pulmonary arteries. (2) Pulmonary inflammation is closely correlated to cigarette smoking and clinical parameters such as BODE index, FEV1%pred and 6MWD.It is one of the key factors affecting the progression of COPD.