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  • Title: [Nitric oxide in the treatment of COPD-induced chronic cor pulmonale: therapeutic effect and mechanism].
    Author: Zhang H, Pang B, Guo S.
    Journal: Zhonghua Yi Xue Za Zhi; 1998 May; 78(5):347-9. PubMed ID: 10923437.
    Abstract:
    OBJECTIVE: To study the hemodynamic and oxygen-dynamic effects and the mechanism of nitric oxide (NO) inhalation therapy in COPD-induced chronic cor pulmonale at acute exacerbation period. METHOD: Right heart catheterization was performed in 11 cases of chronic cor pulmonale. The hemodynamic parameters and plasma endothelium-I(ET-I) level were examined and recorded before and after inhalation of 40 ppm NO for 20 minutes. The plasma level of NO and lipid peroxide Ca(2+)-Mg(2+)-ATPase(calcium pump) and Na(+)-K(+)-ATPase (natrium pump) activities of RBC membrane in 30 cases of chronic cor pulmonale and 30 healthy controls were determined synchronously. RESULTS: After NO therapy, the average pulmonary pressure (PAPM) and pulmonary vascular resistance index (PVRI) were lowered by 16.6% and 25.9% respectively (P < 0.05). Intrapulmonary shunt was lowered by 16.3% (P < 0.05). ET-I also lowered and showed a positive correlation with PAPM (r = 0.59, P < 0.05). The activities of calcium and natrium pump were lowered when NO level declined, showing a positive correlation with NO concentration and negative correlation with lipid peroxides. CONCLUSION: No inhalation therapy exerted favorable hemodynamic and oxygen-dynamic effects on COPD-induced chronic cor pulmonale in its exacerbation period. Suppression of ET-I release might be one of the important factors for pulmonary vessel relaxation. Dysfunction of calcium and natrium pump activities in the acute exacerbation period of chronic cor pulmonale were closely related to NO level.
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