The inhibition of pulmonary vessel remodeling by carbon monoxide system in rats with chronic pulmonary heart disease.

Author(s): Huang X, Wang L, Chen S, Xu Z, Wang Q, Fan X

Affiliation(s): Department of Respirology First Hospital, Institute of Cor Pulmonale, Wenzhou Medical College, Wenzhou 325003, China.

Publication date & source: 2002-07, Zhonghua Jie He He Hu Xi Za Zhi., 25(7):408-11.

Publication type:

OBJECTIVE: To study the effect of carbon monoxide on pulmonary vessel remodeling of chronic pulmonary heart disease. METHODS: Thirty-six sprague-dawley rats were randomly divided into three groups: control group, and hypoxic hypercapnic group, and hypoxic hypercapnia + hemin group. Blood CO concentration (COHb%), activity of HO-1 in blood serum and lung homogenate, pulmonary arteriole micromorphometric index, HO-1 and HO-1 mRNA were measured. RESULTS: (1) mPAP and RV/(LV + S) were (20.1 +/- 0.8) mm Hg and (35.5 +/- 1.7)% in hypoxic hypercapnic group, they were significantly higher than those of control group's (15.3 +/- 1.4) mm Hg, (26.7 +/- 1.7)%, and those of hypoxic hypercapnia + hemin (activator of HO-1) group's (16.5 +/- 3.7) mm Hg, (30.2 +/- 1.6)% (P < 0.01). (2) Pulmonary arteriole micromorphometric index in rats of hypoxic hypercapnic group were significantly higher than those of control group and hypoxic hypercapnia + hemin group (P < 0.01). (3) Blood CO concentration, activity of HO-1 in blood serum and lung homogenate, content of HO-1 and HO-1 mRNA in pulmonary arterioles in rats of hypoxic hypercapnic group were (2.1 +/- 0.9)%, (73 +/- 18) nmol.L(-1).h(-1), (1 751 +/- 311) pmol.mg(-1).h(-1), 0.191 +/- 0.012 and 0.301 +/- 0.017, were significantly higher than those of control group: (0.5 +/- 0.3)%, (25 +/- 8) nmol.L(-1).h(-1), (385 +/- 46) pmol.mg(-1).h(-1), 0.059 +/- 0.005, 0.131 +/- 0.011, but were significantly lower than those of hypoxic hypercapnia + hemin group: (4.9 +/- 2.1)%, (132 +/- 39) nmol.L(-1).h(-1), (2 849 +/- 426) pmol.mg(-1).h(-1), 0.272 +/- 0.013, 0.339 +/- 0.020 (P < 0.01). (4) Correlation analysis revealed that the relationship between carbon monoxide system and pulmonary arteriole micromorphometric index was significantly negative (P < 0.01). CONCLUSION: Up-regulation of endogenous carbon monoxide system can inhibit pulmonary vessel remodeling in rats with chronic pulmonary heart disease induced by hypoxia and hypercapnia.