血小板活化因子一氧化氮合酶与肺动脉高压的发生关系

The Relationship between Platelet-activating Factor(PAF),Nitric Oxide Synthase(NOS) and Pulmonary Arterial Hypertension(PAH)

目的了解血小板活化因子、一氧化氮合酶与肺动脉高压的发生关系。方法选取COPD导致的肺动脉高压患者30例(A组)、原发性肺动脉高压患者20例(B组)、COPD肺动脉压正常患者30例(C组)、健康对照者30例(D组)。采用双抗夹心ELISA法检测PAF,采用化学比色法测定血清NOS活力。结果 A组、B组的PAF、iNOS水平明显高于C组、D组。A组、B组的cNOS水平明显低于C组、D组,同时A组明显高于B组,相关性分析表明,cNOS与A组和B组的肺动脉压存在显著地负性相关关系。结论 PAF在肺动脉高压的形成中可能发挥一定的作用,但肺动脉压并不随着PAF水平的提高而增加。cNOS水平与肺动脉压存在显著的负性相关关系,cNOS水平降低促进肺动脉高压的发生,且其对COPD导致的肺动脉高压及原发性肺动脉高压的影响程度不同。

Objective To understand the relationship between platelet - activating factor, nitric oxide synthase and pulmonary hypertension. Methods 30 cases of patients with pulmonary hypertension caused by COPD （ group A）, 20 cases of patients with primary pulmonary hypertension （group B） , the COPD pulmonary artery pressure of 30 patients （ group C）, 30 cases of healthy controls （ Group D）. PAF was detected by Double - antibody sandwich ELISA assay. Chemical colorimetric determination was used for serum NOS activity. Results The PAF and iNOS levels in group A and group B were significantly higher than in group C and D group. The cNOS levels in Group A and group B were significantly lower than that in group C and Group D, while group A was significantly higher than the B group. Correlation analysis showed that cNOS had significant negative correlation with group A and group B pulmonary artery pressure. Conclusion Conclusion： PAF may play a role in pulmonary hypertension. However, pulmonary artery pressure increase does not raise the level of PAF. The levels of cNOS and pulmonary artery pres- sure significantly have negative correlation, cNOS reduce the promotion of pulmonary hypertension and it has dif- ferent inference in COPD lead to pulmonary hypertension and primary pulmonary hypertension.