血小板活化因子一氧化氮合酶与肺动脉高压的发生关系

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。

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

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 pressure significantly have negative correlation.cNOS reduce the promotion of pulmonary hypertension and it has different inference in COPD lead to pulmonary hypertension and primary pulmonary hypertension.