Plasma endothelin-1 level in chronic obstructive pulmonary disease: Relationship with natriuretic peptide
Plasma endothelin-1 level in chronic obstructive pulmonary disease: Relationship with natriuretic peptide
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DOI：
10.1159/000029380
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发表时间：
1999-05-01
期刊：
影响因子：
3.7
通讯作者：
Yoshikawa, J
中科院分区：
文献类型：
--
作者：
Fujii, T;Otsuka, T;Yoshikawa, J
背景与目的：内皮素-L(ET-1)是一种由血管内皮细胞产生的强缩血管活性多肽。本研究旨在探讨ET-1在慢性阻塞性肺疾病(COPD)继发肺动脉高压中的病理生理作用。方法测定COPD患者右心导尿术中静息状态、运动状态和吸氧状态下血浆ET-1水平。同时测定血浆心钠素(ANP)和脑利钠肽(BNP)水平。结果：21例慢性阻塞性肺疾病患者静息时血浆ET-L水平显著高于16例正常对照组(p<；0.001)。COPD患者静息状态下血浆ET-1水平与肺动脉压、肺血管阻力无相关性。血浆ET-1水平与混合静脉血氧分压呈显著负相关(r=-0.503，p<；0.05)。血浆ET-1水平与心钠素(r=0.540，P<0.05)、脑钠素(r=0.533，P<0.05)呈正相关。吸氧显著降低静息状态下血浆ET-1水平(p<；0.05)。尽管出现了肺动脉高压和低氧血症的进展，但运动对血浆ET-1水平没有显著影响。相反，随着运动的进行，血浆ANP和BNP水平均显著升高(p<；0.01)。结论：COPD患者血浆ET-1水平不受运动中急性进展的肺动脉高压和低氧血症的影响，持续性低氧血症可能与血浆ET-1水平升高有关。此外，我们的研究结果提示，在这些患者中，ANP和BNP可能通过与ET-1相互作用来调节肺血管张力。
Background and Objective: Endothelin-l (ET-1) is a potent vasoconstrictor peptide produced by the vascular endothelium. The purpose of this study was to elucidate the pathophysiological role of ET-1 in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD). Method We measured plasma ET-1 levels during right heart catheterization both at rest and during exercise on room air and while breathing oxygen in patients with COPD. In addition, we simultaneously measured plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Results: Plasma ET-l levels at rest were significantly higher in 21 patients with COPD than in 16 control subjects (p < 0.001). For COPD patients, there was no correlation between the plasma ET-1 level and pulmonary arterial pressure or pulmonary vascular resistance at rest. On the other hand, there was a significant negative correlation between plasma ET-1 level and mixed venous oxygen tension (r = -0.503, p < 0.05). Also, the plasma ET-1 level was positively correlated with those of ANP (r = 0.540, p < 0.05) and BNP (r = 0.533, p < 0.05) at baseline. Oxygen administration significantly decreased plasma ET-1 levels at rest (p < 0.05). Plasma ET-1 levels did not change significantly with exercise despite the progression of pulmonary hypertension and hypoxemia. In contrast, plasma ANP and BNP levels both increased markedly with exercise (p < 0.01). Conclusion: We conclude that in patients with COPD, the plasma ET-1 level is not affected by acute progression of pulmonary hypertension and hypoxemia during exercise, and persistent hypoxemia may be associated with an increase in the plasma ET-1 level. In addition, our findings suggest that ANP and BNP may modulate the pulmonary vascular tone by interacting with ET-1 in these patients.