高原地区慢性阻塞性肺疾病患者血清C反应蛋白、内皮素1与脑钠肽的变化及其对肺动脉高压的影响

Serum C-reaction protein,endothelin-1 and brain natriuretic peptide in patients with chronic obstructive pulmonary disease in plateau region and pulmonary hypertension

目的探讨高原地区慢性阻塞性肺疾病(COPD)患者血清C反应蛋白(CRP),脑钠肽(BNP);内皮素-1(ET-1)的浓度,及与不同程度肺动脉高压(PH)的关系。方法采用多普勒心脏超声对COPD患者118例测定肺动脉压,根据肺动脉压力将其分为3组,无肺动脉高压组(COPD-NPH),轻度PH组(COPD-mPH),中重度PH组(COPD-sPH),以酶联免疫吸附测定(ELISA)法测定CRP及ET-1,免疫荧光法测定BNP。结果随着PH的增加,PO_2明显降低,3组间差异有统计学意义(P<0.05)。COPD-sPH患者血红蛋白(HB)及血细胞比容(HCT)显著高于COPD-mPH患者及无PH患者(F=10.672,F=6.383,P均<0.05)。3组中CRP、BNP、ET-1差异有统计学意义(P均<0.01),肺动脉收缩压(sPAP)与血清CRP(r=0.354,P=0.000)及BNP(r=0.427,P=0.000);及ET-1(r=0.453,P=0.000)水平有显著性相关。结论高原COPD患者低氧血症更严重,HB及HCT异常增加,血液学的高凝状态,促进了PH的形成。血浆CRP水平随着肺动脉压的升高而增加,提示全身炎症可能参与了COPD继发肺动脉高压的形成;CRP,ET-1,BNP共同参与了COPD继发肺动脉高压发生和发展。

Objective To investigate the levels of plasma C-reactive protein（CRP）,brain natriuretic peptide （BNP）, endothelialin-1（ET-1） and pulmonary hypertension（PH） in the patients with chronic obstructive pulmonary disease（COPD） in the plateau region. Methods A total of 118 patients with COPD were included. Pulmonary artery pressure was measured by Doppler echocardiogram. CRP, BNP and ET-1 were tested by ELISA. All the patients were divided into three groups： COPD non-PH（COPD-nPH group）,COPD with mild PH（COPD-mPH group）, COPD with serious PH（COPD-sPH） group serious.Results As pulmonary artery pressure increased, PO2 decreased, there were significantly differences among three groups （P〈0.05）. Hb and HCT in COPDsPH group were significantly higher than those of COPD-mPH （F=10.672,P〈0.05） and COPDNPH group （F=6.383,P〈0.05）. There were also significant differences in the levels of CRP, BNP, and ET-1 among three groups（P〈0.01）. Pulmonary artery systolic pressure was positively associated with CRP （r=0.354,P=0.000）, BNP （r=0.427,P=0.000）, and ET-1 （r=0.453,P=0.000）.Conclusion The patients with COPD in the plateau region have worse hypoxemia, greater abnormal Hb and HCT, and higher condensation state of blood, which promotes pulmonary arterial pressure. As the pulmonary artery pressure increases, the plasma CRP increases, suggesting systemic inflammation may be involved in the PH induced by COPD.