Endogenous hydrogen sulfide in patients with COPD
Endogenous hydrogen sulfide in patients with COPD
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DOI：
10.1378/chest.128.5.3205
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发表时间：
2005-11-01
期刊：
影响因子：
9.6
通讯作者：
Tang, CS
中科院分区：
文献类型：
--
作者：
Chen, YH;Yao, WZ;Tang, CS
目的：慢性阻塞性肺疾病（COPD）是一种以进行性气道阻塞为特征的疾病。近年来的研究表明，内源性硫化氢（H2S）可能是除一氧化氮（NO）和一氧化碳（CO）外的第三种信号气体递质。为探讨内源性H、S在COPD发病中的作用，本研究采用肺功能和气道炎症指标，检测了27例COPD急性加重期（AECOPD）患者、37例稳定期COPD患者和13例健康对照者血清H2S、NO水平、肺功能和诱导痰细胞分类计数。AECOPD患者测量动脉血气水平并接受多普勒超声心动图检查。此外，为了阐明年龄和吸烟状况对血清H2S水平的影响，我们招募了三组与研究组年龄匹配但没有气流刺激的人结果：血清H2S水平（34.0 +/- 0.9至36.4 +/- 1.1 μ mol/L [+/- SEM]）在不同年龄（分别为56.6至75.0岁）的健康对照受试者中无差异。稳定期COPD患者血清H2S水平显著高于AECOPD患者和年龄匹配的对照组（p < 0.01），并与所有健康对照组和所有COPD患者的NO水平呈正相关（r = 0.352，p = 0.000）。吸烟者血清H2S水平显著低于非吸烟者，AECOPD组（p < 0.05）和健康对照组（p < 0.01）。AECOPD组吸烟者的血清CRP水平显著低于健康吸烟者和COPD稳定期吸烟者（P < 0.01）。COPD稳定期患者血清H_2S水平随气道阻塞程度不同而降低（p <0.05），Ⅲ期患者血清H_2S水平低于Ⅰ期患者（p < 0.05）。COPD患者和健康对照组血清H2S水平与FEV 1预测值百分比呈正相关（r = 0.300，p = 0.009）。肺动脉收缩压（PASP）≥ 35 mm Hg的AECOPD患者，其肺动脉收缩压明显低于PASP正常者（P < 0.05），且与PASP呈负相关（r =-0.561，P = 0.011）。血清H2S水平与中性粒细胞比例呈负相关，（r =-0.422，p = 0.001），与淋巴细胞比例呈正相关（r = 0.286，p = 0.028）和尼亚克龙（r = 0.334，p = 0.01）。结论：内源性H2S参与了COPD气道阻塞的发病机制，其水平的变化可能与疾病的活动性和严重程度有关。
Objectives: COPD is characterized by progressive airway obstruction. Recent studies showed that besides nitric oxide (NO) and carbon monoxide (CO), endogenous hydrogen sulfide (H2S) might be the third signaling gasotransmitter. To clarify the role of endogenous H,S in the pathogenesis of COPD, we investigated the relation of serum H2S level to severity of COPD as defined by lung function and airway inflammation.Methods: Levels Of Serum H2S and NO, lung function, and cell differential counts in induced sputum were studied in 27 patients with acute exacerbation of COPD (AECOPD), 37 patients with stable COPD, and 13 healthy subjects. Patients with AECOPD had arterial blood gas levels measured and underwent Doppler echocardiography. In addition, in order to clarify the effects of age and smoking status on serum H2S level, we recruited three groups who were age matched to the study group but had no airflow hinitation (59 subjects).Results: Serum H2S level (34.0 +/- 0.9 to 36.4 +/- 1.1 mu mol/L [+/- SEM]) did not differ among healthy control subjects with different ages (56.6 to 75.0 years, respectively). Serum H2S level was significantly higher in patients with stable COPD than in patients with AECOPD and age-matched control subjects (p < 0.01) and correlated positively with NO level in all healthy control subjects and all patients with COPD (r = 0.352, p = 0.000). Serum H2S level was significantly lower in smokers than nonsmokers, both with AECOPD (p < 0.05) and healthy control subjects (p < 0.01). It was significantly lower in smokers with AECOPD than healthy smokers and smokers with stable COPD (p < 0.01). Serum H2S level differed and was decreased (p < 0.05) among stable COPD patients by stage of airway obstruction (p < 0.05), and it was lower in patients with stage III than stage I obstruction (p < 0.05). Serum H2S level in all patients with COPD and healthy control subjects con-elated positively with the percentage of predicted FEV1 value (r = 0.300, p = 0.009). It was lower in patients with AECOPD and systolic pulmonary artery pressure (PASP) >= 35 mm Hg than those with PASP within the normal range (< 35 mm 14g) [p < 0.05] and was negatively correlated with PASP (r = - 0.561, p = 0.011). Serum H2S level was negatively correlated with proportion of neutrophils in sputuni (r = -0.422, p = 0.001) and positively correlated with proportion of lymphocytes (r = 0.286, p = 0.028) and niacrophages (r = 0.334, p = 0.01) in all patients with COPD.Conclusions: Endogenous H2S is involved in the pathogenesis of airway obstruction in COPD, and its alteration in level may be connected with disease activity and severity.