The
COPD model was established with an
elastase drip into the trachea combined with smoking. The cold-dryness
COPD model was developed by stressing with a cold-dry environment. Success of the model was determined by observation of pathologic lung sections. Rats were sacrificed by
exsanguination from the femoral artery and changes of peripheral blood CD4+, CD8+, and CD4+/CD8+ were detected by flow cytometry. Data were analyzed with SAS 11.5 statistical software.
RESULTS: On the ninetieth day after ending the experiment, Peak expiratory flow in the cold-dryness
COPD group was lower than that in the
COPD and normal control groups (P < 0.01). The time of inspiration in the cold-dryness
COPD group was higher than that in the
COPD and normal groups (P < 0.05). Time of expiration (Te) in the cold-dryness
COPD group was higher than that in the
COPD and normal groups (P < 0.01). 50% tidal volume expiratory flow (EF50) in the cold-dryness
COPD group was lower than that in the
COPD and normal groups (P < 0.01), and EF50 in the
COPD group was lower than that in the normal group (P < 0.05). CD4+ content of peripheral blood in the cold-dryness
COPD group was lower than that in the
COPD and the normal groups (P < 0.05). CD8+ content in the cold-dryness
COPD and
COPD groups was higher than that in the normal control group (P < 0.01), and CD8+ content in the cold-dryness
COPD group was higher than that in the
COPD group (P < 0.01). CD4+/CD8+ in the cold-dryness
COPD group and the
COPD group was lower than that in the normal control group (P < 0.01), and CD4+/CD8+ in the cold-dryness
COPD group was lower than that in the
COPD group (P < 0.05).
CONCLUSION: In the cold-dryness
COPD model, CD8+ increased and CD4+/CD8+ decreased. Moreover, cold-dryness may aggravate this state. The effects of cold-dryness on pulmonary function mainly manifested as prolongation of Te and decrease of EF50, which could be one of causes of cold-dryness environment in the northwest of China leading to
COPD with region characteristics.