Relationship Between Endogenous Hydrogen Sulfide and Pulmonary Vascular Indexes on High-Resolution Computed Tomography in Patients with Chronic Obstructive Pulmonary Disease

OBJECTIVE: To explore the relationship between endogenous hydrogen sulfide (H(2)S) and high-resolution computed tomography (HRCT) indexes in pulmonary vascular remodeling. METHODS: A total of 94 stable chronic obstructive pulmonary disease (COPD) patients were recruited for the study．Plasma H(2)S levels were measured using fluorescence probe. Fluorescence quantitative polymerase chain reaction was used to measure H(2)S synthase cystathionine-γ-lyase (CSE) mRNA and cystathionine-β-synthesis enzyme (CBS) mRNA. The main pulmonary artery diameter (mPAD), axial diagonal mPAD, coronal mPAD, sagittal mPAD, right pulmonary artery diameter (RPAD), left pulmonary artery diameter (LPAD), and ascending aortic diameter (AAD) and the percentage of total cross-sectional area of vessels less than 5 mm(2) of total lung area (%CSA <5) on HRCT were measured. Pulmonary arterial systolic pressure (PASP) of echocardiography, blood gas analysis, and routine blood tests were performed. Correlation analysis and multivariate linear regression were performed using SPSS 22.0. RESULTS: H(2)S was negatively correlated with mPAD, axial diagonal mPAD, and sagittal mPAD (r = −0.25~−0.32) and positively correlated with PaO(2) (r = 0.35). Relative expression of CSE mRNA was positively correlated with PASP, coronal mPAD, sagittal mPAD, white blood cell count (WBC), and neutrophil count (N) (r = 0.30~0.44). The relative expression of CBS mRNA was positively correlated with PASP, WBC, and N (r = 0.34~0.41). In separate models predicting pulmonary vascular indexes, a 1μmol/L increase in H(2)S predicted lower pulmonary artery diameter (for axial diagonal mPAD, 0.76mm lower; for mPAD/AAD, 0.68mm lower). All P values were less than 0.05. CONCLUSION: Endogenous H(2)S may be involved in pulmonary vascular remodeling, providing a new method for the diagnosis and treatment of COPD. The generation of H(2)S may be inhibited by hypoxia, inflammation, etc.