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Endogenous hydrogen sulfide in patients with COPD.
Ya-Hong Chen1, Wan-Zhen Yao, Bin Geng
1Respiratory Department, Peking University, Third Hospital, Beijing, ROC. chenyahong@vip.sina.com
Chest
|November 24, 2005
Summary
Endogenous hydrogen sulfide (H(2)S) levels are altered in chronic obstructive pulmonary disease (COPD), correlating with disease severity and airway inflammation. Lower H(2)S levels are observed in smokers and during acute exacerbations.
Area of Science:
- Pulmonary Medicine
- Biochemistry
- Gasotransmitter Signaling
Background:
- Chronic obstructive pulmonary disease (COPD) involves progressive airway obstruction.
- Endogenous hydrogen sulfide (H(2)S) is recognized as a third signaling gasotransmitter alongside nitric oxide (NO) and carbon monoxide (CO).
Purpose of the Study:
- To investigate the relationship between serum H(2)S levels and the severity of COPD.
- To assess the correlation of H(2)S with lung function and airway inflammation in COPD patients.
Main Methods:
- Measured serum H(2)S and NO levels, lung function, and sputum cell differentials in stable COPD, acute exacerbation of COPD (AECOPD), and healthy controls.
- Included age-matched healthy subjects to evaluate age and smoking effects.
- Assessed arterial blood gas and Doppler echocardiography in AECOPD patients.
Main Results:
- Serum H(2)S was higher in stable COPD patients than in AECOPD patients and controls.
- H(2)S levels were lower in smokers and decreased with increasing airway obstruction severity (Stage III vs. Stage I).
- H(2)S correlated positively with NO and FEV1, and negatively with neutrophils and pulmonary artery pressure.
Conclusions:
- Endogenous H(2)S plays a role in the pathogenesis of COPD.
- Alterations in serum H(2)S levels are associated with COPD disease activity and severity.