[The expression of prostacyclin in lungs from patients with chronic obstructive pulmonary disease].

OBJECTIVE

to investigate the expression of prostacyclin in lungs from patients with chronic obstructive pulmonary disease (COPD).

METHODS

the lung tissues were obtained from 12 patients with COPD and 10 patients without COPD. The apoptosis of pulmonary vascular endothelial cells was analyzed quantitatively using TdT-mediated dUTP nick end labeling (TUNEL). The expression of PGI2-S protein was assessed by immunohistochemistry of paraffin-embedded tissues. 6-keto Prostaglandin F1a, the stable metabolite of PGI2, was measured by enzyme-linked immunosorbent assay in whole-lung tissue extracts. The data distributed normally were expressed as x(-) +/- s, and the independent-samples t test was used for comparison of means.

RESULTS

the apoptotic index (AI) of endothelial cells of medium and small-sized vessels in patients with COPD group [(12.9 +/- 2.0)%, (11.4 +/- 1.4)%] were significantly higher than that of patients without COPD [(6.1 +/- 1.2)%, (5.9 +/- 0.4)%]. In patients without COPD, PGI2-S protein expression in medium vessels and small-sized vessels was (95.4 +/- 2.1)% and (82.3 +/- 7.4)% respectively, and the value was (95.5 +/- 2.2)% in airway epithelial cells. In patients with COPD, PGI2-S expression in medium vessels and small-sized vessels decreased remarkably [(55.2 +/- 9.8)% and (42.3 +/- 5.1)% respectively], and exhibited a marked reduction in airway epithelial cells (31.8 +/- 5.2)%. The level of 6-keto Prostaglandin F1a was significantly lower in patients with COPD (2.6 +/- 0.4)microg/L compared with patients without COPD (16.2 +/- 2.8)microg/L.

CONCLUSION

abnormal apoptosis exists in pulmonary vascular endothelial cells in patients with COPD. In patients with COPD, the expression of PGI2-S and the level of 6-keto Prostaglandin F1a in lung tissues were decreased. The results suggest that abnormal apoptosis, reduction of PGI2-S expression and PGI2 may be important histological markers for pulmonary endothelial cell dysfunction in COPD and may be involved in the pathogenesis of the disease.