Objective To explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension(PAH) in patients of chronic obstructive pulmonary disease(COPD) associated with chronic cor pulmonale(C...Objective To explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension(PAH) in patients of chronic obstructive pulmonary disease(COPD) associated with chronic cor pulmonale(CCP) during exacerbation.Methods Seventy patients of COPD and CCP with acute exacerbation were randomly and equally divided into control group and treatment group.The control group received standard treatment with antibiotics,antiasthmatic and expectorant medications,and oxygenation;and the ligustrazine treatment group received ligustrazine treatment(80 mg/d;i.v.;for 2 weeks) in addition to the standard treatment.Before and at the end of 2 week treatment,the clinic responses of the two regimens were evaluated,plasma levels of endothelin-1(ET-1) and nitric oxide(NO) were determined;arterial oxygen partial pressure(PaO_2),mean pulmonary arterial pressure(mPAP),outflow tract of right ventricle(RVOT),and internal diameter of right ventricle(RV) were measured.Results Good clinic benefits were achieved in both the standard and ligustrazine regimens,plasma level of ET-1,values of mPAP,RV and RVOT decreased significantly,plasma level of NO and PaO_2 values decreased(all P<0.01 vs pretreatment to all parameters).Compared with the control group,ligustrazine greatly enhanced the clinic efficacy from 77.1%to 97.1%(P<0.05),and also resulted in more significant changes of all these parameters(P<0.01 vs control group for all parameters).For both groups,the levels of plasma ET-1 were positively correlated with values of mPAP,RVOT,and RV(r = 0.710,0.853,and 0.766,respectively,all P = 0.000),and negatively correlated with plasma NO and PaO_2(r =- 0.823,and- 0.752,respectively,all P = 0.000).Conclusion Ligustrazine is effective in treating pulmonary artery hypertension during acute exacerbation of COPD and CCP in patients from the plateau area.The observed changes in the plasma levels of NO and ET-1 in response to ligustrazine treatment suggest that ligustrazine may act through the selective effect on pulmonary blood vessels to enhance the synthesis and release of NO and suppress those of ET-1 from lung vascular endothelial cells,thus reducing pulmonary artery pressure and decreasing pulmonary arterial hypertension.展开更多
Objective To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods Twent...Objective To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods Twenty patients with simple ventricular septal defect (VSD) were chosen as controls, and 30 patients with PH were studied. Plasma levels of ET-1 and NO were measured by radioimmunoassay or colorimetric method. Before cardiopulmonary bypass was established, the specimens from right lung were fixed with formaldehyde solution, embedded with paraffin and stained by SP immunohistochemistry. Intercellular adhesion molecule-1 (ICAM-1) expression was measured through the determination of the light density with computer imaging technology. Results Compared with that of the patients with simple VSD, the light density of ICAM-1 and plasma level of ET-1 increased in patients with PH; but plasma level of NO decreased (P<0.05). Positive correlation was observed between ICAM-1 and ET-1/NO (P<0.05). Conclusion Endothelia cells activation and imbalance of ET-1/NO might play an important role in the development of PH.展开更多
Background:Reversibility of pulmonary hypertension(PH)is closely related to the treatment options for and prognosis of children with congenital heart disease.Objective:We combined patient-specific clinical features in...Background:Reversibility of pulmonary hypertension(PH)is closely related to the treatment options for and prognosis of children with congenital heart disease.Objective:We combined patient-specific clinical features including diagnosis,age and echocardiographic results,and biomarkers of pulmonary vascular dysfunction to explore the noninvasive methods that can be used to accurately evaluate the reversibility of pulmonary hypertension in congenital heart disease(PH-CHD).Methods:Based on the preoperative systolic pulmonary arterial pressure(sPAP),70 CHD patients were divided into normal,PH-CHD suspected,and confirmed groups.Additionally,biomarkers of circulating endothelial cells(CECs),endothelin-1(ET-1),and endothelial nitric oxide synthase(eNOS)were detected.Patients were categorized into reversible(RPH)and irreversible(IRPH)groups according to the sPAP 6 months after surgery.Risk stratification was performed according to the clinical features and biomarkers.Results:CECs and ET-1 levels in the confirmed group were significantly higher.eNOS was higher in the confirmed and suspected groups than that in the normal group.CECs in the IRPH group were significantly higher compared to the RPH group.No such intergroup differences were observed with respect to ET-1 and eNOS levels.The ROC curve showed that the risk stratification was of high diagnostic value to evaluate reversibility.Conclusion:The CECs,eNOS,and ET-1 were closely related with PH-CHD.CECs and risk stratification have high practical value in assessing the reversibility of PH-CHD.展开更多
Objective: To study the effects of serum Fractalkine on vascular remodeling and oxidative stress activation in patients with COPD complicated by pulmonary heart disease. Methods:Patients who were hospitalized in Chong...Objective: To study the effects of serum Fractalkine on vascular remodeling and oxidative stress activation in patients with COPD complicated by pulmonary heart disease. Methods:Patients who were hospitalized in Chongqing Armed Corps Police Hospital due to COPD between June 2014 and April 2017 were selected, the patients with COPD alone were included in COPD group, and the patients with COPD complicated by pulmonary heart disease were included in COPD+PHD group;healthy volunteers who underwent physical examination during the same period were selected as the control group of the study. The serum was collected to determine the contents of Fractalkine, vascular remodeling indexes and oxidative stress indexes. Results: Serum Fractalkine, ANG-2, MMP2, MMP9, VEGF, FGF2, Nogo-B, ET-1 and MDA contents of COPD+PHD group and COPD group were higher than those of control group whereas T-AOC contents were lower than that of control group;serum Fractalkine, ANG-2, MMP2, MMP9, VEGF, FGF2, Nogo-B, ET-1 and MDA contents of COPD+PHD group were higher than those of COPD group whereas T-AOC content was lower than that of COPD group. Serum ANG-2, MMP2, MMP9, VEGF, FGF2, Nogo-B, ET-1 and MDA contents of COPD+PHD group of patients with high Fractalkine content were significantly higher than those of COPD+PHD group of patients with low Fractalkine content whereas T-AOC content was lower than that of COPD+PHD group of patients with low Fractalkine content. Conclusion: The increase of serum Fractalkine in patients with COPD complicated by pulmonary heart disease can aggravate the vascular remodeling and promote the oxidative stress activation.展开更多
Background Exhaled nitric oxide （NO） is a noninvasive biomarker of airway inflammation in pulmonary diseases. Hydrogen sulfide （H2S）, as the third member of the gasotransmitter family, is involved in the pathophys...Background Exhaled nitric oxide （NO） is a noninvasive biomarker of airway inflammation in pulmonary diseases. Hydrogen sulfide （H2S）, as the third member of the gasotransmitter family, is involved in the pathophysiological process in lung diseases. H2S also exists in exhaled breath and can be sampled non-invasively. The study investigated the level of exhaled H2S in patients with chronic obstructive pulmonary disease （COPD） and its correlation with exhaled NO. Methods Levels of exhaled NO and H2S, lung function, and cell differential counts in induced sputum were studied in 19 patients with acute exacerbation of COPD （AECOPD）, 19 patients with stable COPD and seven healthy smoke controls. Results Exhaled H2S levels were similar in patients with AECOPD （10.0 parts per billion （ppb）, 8.0-13.0 ppb）, stable COPD （10.0 ppb, 9.0-12.0 ppb）, and healthy controls （9.0 ppb, 8.0-16.0 ppb） （P 〉0,05）. Exhaled NO levels were similar in patients with AECOPD （155.0 ppb, 129.0-190.0 ppb）, stable COPD （154.0 ppb, 133.0-175.0 ppb） and healthy controls （165.0 ppb, 112.0-188.0 ppb） （P 〉0.05）. Exhaled H2S levels correlated positively with exhaled NO in all healthy controls and patients with COPD （r=0.467, P 〈0.01）. No significant correlation was found between the exhaled H2S level and percentage of predicted FEV1 （P 〉0.05） and proportion of different cell types in induced sputum （P 〉0.05）. Conclusions There is a correlation between exhaled H2S and exhaled NO. The role of exhaled H2S in airway inflammation in COPD still needs further investigation.展开更多
Background：It has been demonstrated that only 10%-20% cigarette smokers finally suffer chronic obstructive pulmonary disease （COPD）.The underlying mechanism of development remains uncertain so far.Nitric oxide （NO...Background：It has been demonstrated that only 10%-20% cigarette smokers finally suffer chronic obstructive pulmonary disease （COPD）.The underlying mechanism of development remains uncertain so far.Nitric oxide （NO） has been found to be closely associated with the pathogenesis of COPD,the alteration of NO synthase （NOS） expression need to be revealed.The study aimed to investigate the alterations of NOS isoforms expressions between smokers with and without COPD,which might be helpful for identifying the susceptibility of smokers developing into COPD.Methods：Peripheral lung tissues were obtained from 10 nonsmoker control subjects,15 non-COPD smokers,and 15 smokers with COPD.Neuronal NOS （nNOS）,inducible NOS （iNOS）,and endothelial NOS （eNOS） mRNA and protein levels were measured in each sample by using real-time polymerase chain reaction and Westem blotting.Results：INOS mRNA was significantly increased in patients with COPD compared with nonsmokers and smokers with normal lung function （P 〈 0.001,P =0.001,respectively）.iNOS protein was also higher in COPD patients than nonsmokers and smokers with normal lung function （P 〈 0.01 and P =0.01,respectively）.However,expressions ofnNOS and eNOS did not differ among nonsmokers,smokers with and without COPD.Furthermore,there was a negative correlation between iNOS protein level and lung function parameters forced expiratory volume in 1 s （FEV1） （% predicted） （r =-0.549,P =0.001） and FEV1/forced vital capacity （%,r =-0.535,P =0.001）.Conclusions：The expression of iNOS significantly increased in smokers with COPD compared with that in nonsmokers or smokers without COPD.The results suggest that iNOS might be involved in the pathogenesis of COPD,and may be a potential marker to identify the smokers who have more liability to suffer COPD.展开更多
Background It has been widely demonstrated that endothelial progenitor cells are involved in several diseases and that they have therapeutic implications. In order to define the altered pulmonary vascular homeostasis ...Background It has been widely demonstrated that endothelial progenitor cells are involved in several diseases and that they have therapeutic implications. In order to define the altered pulmonary vascular homeostasis in chronic obstructive pulmonary disease, we sought to observe the level and functions of circulating endothelial progenitor calls in patients with chronic obstructive pulmonary disease. Methods The total study population included 20 patients with chronic obstructive pulmonary disease and 20 control subjects. The number of circulating endothelial progenitor cells （CD34＋/CD133＋/IVEGFR-2＋cells） was counted by flow cytometry. Circulating endothelial progenitor cells were also cultured in vitro and characterized by uptake of Dil- acLDL, combining with UEA-I, and expression of von Willebrand factor and endothelial nitric oxide synthase. Adhesion, proliferation, production of nitric oxide, and expression of endothelial nitric oxide synthase and phosphorylated-endothelial nitric oxide synthase were detected to determine functions of circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease. Results The number of circulating endothelial progenitor cells in the chronic obstructive pulmonary disease group was lower than in the control group： （0.54±0.16）% vs. （1.15±0.57）%, P 〈0.05. About 80% of adherent peripheral blood mononuclear cells cultured in vitro were double labeled with Dil-acLDL and UEA-I. The 92% and 91% of them were positive for von Willebrand factor and endothelial nitric oxide synthase, respectively. Compared with the control, there were significantly fewer adhering endothelial progenitor cells in chronic obstructive pulmonary disease patients： 18.7±4.8/field vs. 45.0±5.9/field, P 〈0.05. The proliferation assay showed that the proliferative capacity of circulating endothelial progenitor cells from chronic obstructive pulmonary disease patients was significantly impaired： 0.135±0.038 vs. 0.224±0.042, P 〈0.05. Furthermore, nitric oxide synthase （112.06±10.00 vs. 135.41±5.38, P 〈0.05）, phosphorylated endothelial nitric oxide synthase protein expression （88.89±4.98 vs. 117.98±16.49, P 〈0.05） and nitric oxide production （（25.11±5.27） Iμmol/L vs. （37.72±7.10） μmol/L, P 〈0.05） were remarkably lower in endothelial cells from the chronic obstructive pulmonary disease group than the control. Conclusion Circulating endothelial progenitor cells were decreased and functionally impaired in patients with chronic obstructive pulmonary disease.展开更多
基金supported by the Key scientific and technological project in Qinghai Province,China (2006-N-143)
文摘Objective To explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension(PAH) in patients of chronic obstructive pulmonary disease(COPD) associated with chronic cor pulmonale(CCP) during exacerbation.Methods Seventy patients of COPD and CCP with acute exacerbation were randomly and equally divided into control group and treatment group.The control group received standard treatment with antibiotics,antiasthmatic and expectorant medications,and oxygenation;and the ligustrazine treatment group received ligustrazine treatment(80 mg/d;i.v.;for 2 weeks) in addition to the standard treatment.Before and at the end of 2 week treatment,the clinic responses of the two regimens were evaluated,plasma levels of endothelin-1(ET-1) and nitric oxide(NO) were determined;arterial oxygen partial pressure(PaO_2),mean pulmonary arterial pressure(mPAP),outflow tract of right ventricle(RVOT),and internal diameter of right ventricle(RV) were measured.Results Good clinic benefits were achieved in both the standard and ligustrazine regimens,plasma level of ET-1,values of mPAP,RV and RVOT decreased significantly,plasma level of NO and PaO_2 values decreased(all P<0.01 vs pretreatment to all parameters).Compared with the control group,ligustrazine greatly enhanced the clinic efficacy from 77.1%to 97.1%(P<0.05),and also resulted in more significant changes of all these parameters(P<0.01 vs control group for all parameters).For both groups,the levels of plasma ET-1 were positively correlated with values of mPAP,RVOT,and RV(r = 0.710,0.853,and 0.766,respectively,all P = 0.000),and negatively correlated with plasma NO and PaO_2(r =- 0.823,and- 0.752,respectively,all P = 0.000).Conclusion Ligustrazine is effective in treating pulmonary artery hypertension during acute exacerbation of COPD and CCP in patients from the plateau area.The observed changes in the plasma levels of NO and ET-1 in response to ligustrazine treatment suggest that ligustrazine may act through the selective effect on pulmonary blood vessels to enhance the synthesis and release of NO and suppress those of ET-1 from lung vascular endothelial cells,thus reducing pulmonary artery pressure and decreasing pulmonary arterial hypertension.
基金this work was supported by Xi'an Science and technology Research Fund (GG04134)
文摘Objective To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods Twenty patients with simple ventricular septal defect (VSD) were chosen as controls, and 30 patients with PH were studied. Plasma levels of ET-1 and NO were measured by radioimmunoassay or colorimetric method. Before cardiopulmonary bypass was established, the specimens from right lung were fixed with formaldehyde solution, embedded with paraffin and stained by SP immunohistochemistry. Intercellular adhesion molecule-1 (ICAM-1) expression was measured through the determination of the light density with computer imaging technology. Results Compared with that of the patients with simple VSD, the light density of ICAM-1 and plasma level of ET-1 increased in patients with PH; but plasma level of NO decreased (P<0.05). Positive correlation was observed between ICAM-1 and ET-1/NO (P<0.05). Conclusion Endothelia cells activation and imbalance of ET-1/NO might play an important role in the development of PH.
基金We thank the support of National Nature Science Foundation of China(81771934)Shanghai Jiao Tong University Medical and Engineering Intersection Fund(YG2019ZDA03).
文摘Background:Reversibility of pulmonary hypertension(PH)is closely related to the treatment options for and prognosis of children with congenital heart disease.Objective:We combined patient-specific clinical features including diagnosis,age and echocardiographic results,and biomarkers of pulmonary vascular dysfunction to explore the noninvasive methods that can be used to accurately evaluate the reversibility of pulmonary hypertension in congenital heart disease(PH-CHD).Methods:Based on the preoperative systolic pulmonary arterial pressure(sPAP),70 CHD patients were divided into normal,PH-CHD suspected,and confirmed groups.Additionally,biomarkers of circulating endothelial cells(CECs),endothelin-1(ET-1),and endothelial nitric oxide synthase(eNOS)were detected.Patients were categorized into reversible(RPH)and irreversible(IRPH)groups according to the sPAP 6 months after surgery.Risk stratification was performed according to the clinical features and biomarkers.Results:CECs and ET-1 levels in the confirmed group were significantly higher.eNOS was higher in the confirmed and suspected groups than that in the normal group.CECs in the IRPH group were significantly higher compared to the RPH group.No such intergroup differences were observed with respect to ET-1 and eNOS levels.The ROC curve showed that the risk stratification was of high diagnostic value to evaluate reversibility.Conclusion:The CECs,eNOS,and ET-1 were closely related with PH-CHD.CECs and risk stratification have high practical value in assessing the reversibility of PH-CHD.
文摘Objective: To study the effects of serum Fractalkine on vascular remodeling and oxidative stress activation in patients with COPD complicated by pulmonary heart disease. Methods:Patients who were hospitalized in Chongqing Armed Corps Police Hospital due to COPD between June 2014 and April 2017 were selected, the patients with COPD alone were included in COPD group, and the patients with COPD complicated by pulmonary heart disease were included in COPD+PHD group;healthy volunteers who underwent physical examination during the same period were selected as the control group of the study. The serum was collected to determine the contents of Fractalkine, vascular remodeling indexes and oxidative stress indexes. Results: Serum Fractalkine, ANG-2, MMP2, MMP9, VEGF, FGF2, Nogo-B, ET-1 and MDA contents of COPD+PHD group and COPD group were higher than those of control group whereas T-AOC contents were lower than that of control group;serum Fractalkine, ANG-2, MMP2, MMP9, VEGF, FGF2, Nogo-B, ET-1 and MDA contents of COPD+PHD group were higher than those of COPD group whereas T-AOC content was lower than that of COPD group. Serum ANG-2, MMP2, MMP9, VEGF, FGF2, Nogo-B, ET-1 and MDA contents of COPD+PHD group of patients with high Fractalkine content were significantly higher than those of COPD+PHD group of patients with low Fractalkine content whereas T-AOC content was lower than that of COPD+PHD group of patients with low Fractalkine content. Conclusion: The increase of serum Fractalkine in patients with COPD complicated by pulmonary heart disease can aggravate the vascular remodeling and promote the oxidative stress activation.
基金This study was supported by a grant from the National Natural Science Foundation of China （No. 81170012）.Acknowledgments： We thank WANG Yu-zhu and HE Yan-jing for technical assistance.
文摘Background Exhaled nitric oxide （NO） is a noninvasive biomarker of airway inflammation in pulmonary diseases. Hydrogen sulfide （H2S）, as the third member of the gasotransmitter family, is involved in the pathophysiological process in lung diseases. H2S also exists in exhaled breath and can be sampled non-invasively. The study investigated the level of exhaled H2S in patients with chronic obstructive pulmonary disease （COPD） and its correlation with exhaled NO. Methods Levels of exhaled NO and H2S, lung function, and cell differential counts in induced sputum were studied in 19 patients with acute exacerbation of COPD （AECOPD）, 19 patients with stable COPD and seven healthy smoke controls. Results Exhaled H2S levels were similar in patients with AECOPD （10.0 parts per billion （ppb）, 8.0-13.0 ppb）, stable COPD （10.0 ppb, 9.0-12.0 ppb）, and healthy controls （9.0 ppb, 8.0-16.0 ppb） （P 〉0,05）. Exhaled NO levels were similar in patients with AECOPD （155.0 ppb, 129.0-190.0 ppb）, stable COPD （154.0 ppb, 133.0-175.0 ppb） and healthy controls （165.0 ppb, 112.0-188.0 ppb） （P 〉0.05）. Exhaled H2S levels correlated positively with exhaled NO in all healthy controls and patients with COPD （r=0.467, P 〈0.01）. No significant correlation was found between the exhaled H2S level and percentage of predicted FEV1 （P 〉0.05） and proportion of different cell types in induced sputum （P 〉0.05）. Conclusions There is a correlation between exhaled H2S and exhaled NO. The role of exhaled H2S in airway inflammation in COPD still needs further investigation.
基金This work was supported by the grants from Natural Science Foundation of China （No. 81270106）, Ministry of Science and Technology of China （No. 2012BA[05B00） and Ministry of Public Health （No. 201002008）.
文摘Background：It has been demonstrated that only 10%-20% cigarette smokers finally suffer chronic obstructive pulmonary disease （COPD）.The underlying mechanism of development remains uncertain so far.Nitric oxide （NO） has been found to be closely associated with the pathogenesis of COPD,the alteration of NO synthase （NOS） expression need to be revealed.The study aimed to investigate the alterations of NOS isoforms expressions between smokers with and without COPD,which might be helpful for identifying the susceptibility of smokers developing into COPD.Methods：Peripheral lung tissues were obtained from 10 nonsmoker control subjects,15 non-COPD smokers,and 15 smokers with COPD.Neuronal NOS （nNOS）,inducible NOS （iNOS）,and endothelial NOS （eNOS） mRNA and protein levels were measured in each sample by using real-time polymerase chain reaction and Westem blotting.Results：INOS mRNA was significantly increased in patients with COPD compared with nonsmokers and smokers with normal lung function （P 〈 0.001,P =0.001,respectively）.iNOS protein was also higher in COPD patients than nonsmokers and smokers with normal lung function （P 〈 0.01 and P =0.01,respectively）.However,expressions ofnNOS and eNOS did not differ among nonsmokers,smokers with and without COPD.Furthermore,there was a negative correlation between iNOS protein level and lung function parameters forced expiratory volume in 1 s （FEV1） （% predicted） （r =-0.549,P =0.001） and FEV1/forced vital capacity （%,r =-0.535,P =0.001）.Conclusions：The expression of iNOS significantly increased in smokers with COPD compared with that in nonsmokers or smokers without COPD.The results suggest that iNOS might be involved in the pathogenesis of COPD,and may be a potential marker to identify the smokers who have more liability to suffer COPD.
基金This work was supported by grants from National Natural Science Foundation of China （No. 81070039, No. 81270100 and No. 81200026） and from the Natural Science Foundation of Hunan Province （No. 2008FJ3152 and No. 2011 SK3237）.
文摘Background It has been widely demonstrated that endothelial progenitor cells are involved in several diseases and that they have therapeutic implications. In order to define the altered pulmonary vascular homeostasis in chronic obstructive pulmonary disease, we sought to observe the level and functions of circulating endothelial progenitor calls in patients with chronic obstructive pulmonary disease. Methods The total study population included 20 patients with chronic obstructive pulmonary disease and 20 control subjects. The number of circulating endothelial progenitor cells （CD34＋/CD133＋/IVEGFR-2＋cells） was counted by flow cytometry. Circulating endothelial progenitor cells were also cultured in vitro and characterized by uptake of Dil- acLDL, combining with UEA-I, and expression of von Willebrand factor and endothelial nitric oxide synthase. Adhesion, proliferation, production of nitric oxide, and expression of endothelial nitric oxide synthase and phosphorylated-endothelial nitric oxide synthase were detected to determine functions of circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease. Results The number of circulating endothelial progenitor cells in the chronic obstructive pulmonary disease group was lower than in the control group： （0.54±0.16）% vs. （1.15±0.57）%, P 〈0.05. About 80% of adherent peripheral blood mononuclear cells cultured in vitro were double labeled with Dil-acLDL and UEA-I. The 92% and 91% of them were positive for von Willebrand factor and endothelial nitric oxide synthase, respectively. Compared with the control, there were significantly fewer adhering endothelial progenitor cells in chronic obstructive pulmonary disease patients： 18.7±4.8/field vs. 45.0±5.9/field, P 〈0.05. The proliferation assay showed that the proliferative capacity of circulating endothelial progenitor cells from chronic obstructive pulmonary disease patients was significantly impaired： 0.135±0.038 vs. 0.224±0.042, P 〈0.05. Furthermore, nitric oxide synthase （112.06±10.00 vs. 135.41±5.38, P 〈0.05）, phosphorylated endothelial nitric oxide synthase protein expression （88.89±4.98 vs. 117.98±16.49, P 〈0.05） and nitric oxide production （（25.11±5.27） Iμmol/L vs. （37.72±7.10） μmol/L, P 〈0.05） were remarkably lower in endothelial cells from the chronic obstructive pulmonary disease group than the control. Conclusion Circulating endothelial progenitor cells were decreased and functionally impaired in patients with chronic obstructive pulmonary disease.
