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目的 探讨白细胞粘附分子在慢性阻塞性肺疾病 (COPD)、慢性肺原性心脏病 (肺心病 )发病机制中的作用 ,及抗白细胞粘附疗法在肺心病治疗中的疗效。方法 采用流式细胞术 ,用单克隆抗体定量测定 42例COPD患者 (稳定期 )、41例肺心病患者 (稳定期 )周围血中白细胞粘附分子CD11a、CD11b、CD18、CD54 的阳性表达率 ,并以 2 4名健康人作正常对照。41例肺心病患者分为 2组 ,治疗组 2 0例 ,服用火把花根片 (1次 3片 ,1日 3次 ) ;对照组 2 1例。测定 2 0例服火把花根片后的肺心病患者周围血中白细胞粘附分子CD11a、CD11b、CD18、CD54 的阳性表达率 ,并与对照组 2 1例肺心病患者作比较。结果 COPD患者组血液单核细胞表面的CD11a、CD11b、CD18、CD54 ,淋巴细胞表面CD11a的阳性表达率明显高于正常对照组 (P <0 0 5 ) ;肺心病患者组血液中性粒细胞表面CD11a、CD11b、CD18、CD54 ,单核细胞表面CD11a、CD18、CD54 ,淋巴细胞表面CD18较正常对照组明显增强 (P <0 0 5 ) ;服火把花根片后 ,肺心病治疗组中性粒细胞表面CD11a、CD11b、CD18、CD54 ,单核细胞表面CD11a、CD18、CD54 ,淋巴细胞表面CD18较服药前肺心病组有显著下降 (P <0 0 5 )。余各型均无显著差异。结论 COPD患者通过单核细胞粘附分子CD11a/CD18、CD11b/C
Objective To investigate the role of leukocyte adhesion molecules in the pathogenesis of chronic obstructive pulmonary disease (COPD) and chronic cor pulmonale (pulmonary heart disease) and the effect of anti-leukocyte adhesion therapy in the treatment of pulmonary heart disease. Methods The expression of leukocyte adhesion molecules CD11a, CD11b, CD18 and CD54 in 42 patients with COPD (stable phase) and 41 patients with chronic cor pulmonale (stable phase) were determined by flow cytometry with monoclonal antibody. And 24 healthy people as a normal control. 41 cases of patients with pulmonary heart disease were divided into two groups, the treatment group 20 cases, taking the torch flower root tablets (1 3 times on the 1st); control group 21 cases. The positive rate of leukocyte adhesion molecules CD11a, CD11b, CD18 and CD54 in the peripheral blood of patients with cor pulmonale treated with Huaganpian tablets was determined and compared with 21 patients with pulmonary heart disease in the control group. Results The positive rates of CD11a, CD11b, CD18, CD54 and CD11a on the surface of mononuclear cells in COPD patients were significantly higher than those in normal controls (P <0.05). The levels of blood neutrophil CD11a, CD11b, CD18, CD54, monocytes CD11a, CD18, CD54, CD18 on lymphocytes were significantly higher than those in normal control group (P <0.05) Cell surface CD11a, CD11b, CD18, CD54, monocyte surface CD11a, CD18, CD54, CD18 on lymphocyte surface were significantly lower than those in the premedication pulmonary heart disease group (P <0.05). I have no significant difference between the various types. Conclusions COPD patients pass monocyte adhesion molecules CD11a / CD18, CD11b / C