ObjectiveTo investigate the effect of azithromycin on chronic obstructive pulmonary disease (COPD) vascular remodeling and its possible mechanism.MethodsEighteen male SD rats were randomly divided into normal control group (group A), model group (group B) and azithromycin intervention group (group C). In group B and group C, the COPD model was established by passive smoking and intratracheal injection of lipopolysaccharide. On the fifteenth day, group C was intragastricly administrated with azithromycin (50 mg/kg) one hour prior to smoking, while group A and group B were given equal amount of normal saline. All the rats were killed 6 weeks later. Hematoxylin-eosin staining was used to observe lung tissue pathological changes and victoria blue + Van Gieson staining was used to observe the pulmonary artery morphology changes. The serum osteopontin (OPN) was determined with ELISA. The protein expression of OPN was measured with immunohistochemistry and OPN mRNA was detected by RT-PCR.ResultsCompared with group A, the degree of pulmonary vascular inflammation and pulmonary vascular remodeling in groups B and C was more serious, but these changes in group C were lighter than those in group B. The serum OPN content, lung tissue OPN protein and OPN mRNA expression in groups B and C were higher than those in group A, while these parameters in group C were lower than those in group B. The content of serum OPN, the expression of OPN protein and OPN mRNA in lung tissue were positively correlated with the degree of pulmonary vascular inflammation and vascular remodeling.ConclusionAzithromycin can alleviate the pulmonary vascular inflammation and pulmonary vascular remodeling in COPD rats, and its mechanism may be related to inhibiting the expression of OPN.
Objective The purpose of the current research was to analyze the relevant risk factors for short-term death in patients with chronic obstructive pulmonary disease (COPD) and heart failure (HF), and to build a predictive nomogram. Methods We conducted a retrospective analysis of clinical data from 1 323 COPD and HF comorbidity patients who were admitted to the Affiliated Hospital of Southwest Medical University from January 2018 to January 2022. Samples were divided into survival and death groups based on whether they died during the follow-up. General data and tested index of both groups were analyzed, and the discrepant index was analyzed by single factor and multiple factor Logistic regression analysis. R software was applied to create the nomogram by visualizing the results of the regression analysis. The accuracy of the results was verified by C index, calibration curve, and ROC curve. Results The results from the multiple factor Logistic regression analysis indicated that age (OR=1.085, 95%CI 1.048 to 1.125), duration of smoking (OR=1.247, 95%CI 1.114 to 1.400), duration of COPD (OR=1.078, 95%CI 1.042 to 1.116), comorbidity with respiratory failure (OR=5.564, 95%CI 3.372 to 9.329), level of NT-proBNP (OR=1.000, 95%CI 1.000 to 1.000), level of PCT (OR=1.153, 95%CI 1.083 to 1.237), and level of D-dimer (OR=1.205, 95%CI 1.099 to 1.336) were risk factors for short-term death of COPD and HF comorbidity patients. The level of ALB (OR=0.892, 95%CI 0.843 to 0.942) was a protective factor that was used to build the predictive nomogram with the C index of 0.874, the square under the working characteristics curve of the samples of 0.874, the specify of 82.5%, and the sensitivity of 75.0%. The calibration curve indicated good predictive ability of the model. Conclusion The nomogram diagram built by the current research indicated good predictability of short-term death in COPD and HF comorbidity patients.