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肺动脉高压是慢性阻塞性肺病 (COPD)的并发症之一 ,在组织学上以血管重建为特征 ,其病因知之甚少。我们曾报道 ,高原地区大鼠重建的肺动脉周围肥大细胞类胰蛋白酶及转化生长因子 β1(TGF β1)免疫组织染色呈高值 ,但COPD患者是否会发生这种改变尚未明了。为阐明此事 ,我们选择 10名严重肺气肿并接受肺容量恢复术的患者作为实验组 ;另选 5名肺周围型癌并接受肺叶切除的患者作为对照组。对肥大细胞类胰蛋白酶及TGF β1的免疫组织化学研究表明 ,COPD肺动脉外径厚度达 10 0～ 2 0 0 μm ,而对照组平均分别为 36.4± 4 .5 %或 2 2 .6± 3%(P <0 .0 5 ) ,COPD患者血管和小气道周围的肥大细胞胰蛋白酶阳性数量与对照组相比显著增加(P <0 .0 1) ,且与血管厚度呈正相关 (r =0 .85 ,P <0 .0 1) ,COPD患者肺中性粒细胞及单核细胞内TGF β1免疫染色呈强阳性 ,但却未在对照组内测到。上述结果表明 ,肥大细胞胰蛋白酶和TGF β1的过量表达可能由气道慢性炎症及低氧血症所致。这两者在COPD患者肺血管重建中起着重要作用
Pulmonary hypertension is one of the complications of chronic obstructive pulmonary disease (COPD), which is histologically characterized by revascularization and its etiology is poorly understood. We have reported that immunohistochemical staining of mast cell tryptase and transforming growth factor-β1 (TGFβ1) around the pulmonary artery in rats at high altitude was high, but it is unclear whether this change occurs in COPD patients. To clarify this, we selected 10 patients with severe emphysema and lung volume recovery surgery as experimental group; 5 patients with lung-type cancer and lobectomy were selected as control group. Immunohistochemical studies of tryptase and TGFβ1 in mast cells showed that the diameter of the pulmonary artery in COPD ranged from 10 to 200 μm, while the control group had an average of 36.4 ± 4.5% or 22.6 ± 3%, respectively (P <0.05). The positive numbers of mast cells in blood vessels and small airways of COPD patients were significantly increased compared with the control group (P <0.01), and positively correlated with the thickness of blood vessel (r = 0. 05). 85, P <0.01). TGF-β1 immunostaining of lung neutrophils and monocytes in COPD patients was strongly positive but not detected in the control group. The above results indicate that overexpression of mast cells trypsin and TGF-β1 may be caused by chronic airway inflammation and hypoxemia. Both of these play an important role in pulmonary vascular remodeling in COPD patients