Zeng G B, Duan S F
Zhonghua Nei Ke Za Zhi. 1989 May;28(5):283-5, 314-5.
The pathogenesis of edema in COPD patients is poorly understood. In 50 COPD patients without cor pulmonale, we measured water sodium and potassium excretion in 24 hours, concentration of sodium and potassium in plasma as well as PRA, ATII and aldosterone levels. We found that PRA, ATII, and aldosterone levels in COPD patients with edema are much higher than those in patients without edema and sodium and water excretion decreased significantly in edematous COPD patients. Elevation of PRA, ATII, and aldosterone correlated with inability to excrete sodium and water. These data suggest that, in conjunction with hypercapnia-hypoxia-mediated disturbance in renal function, stimulation of RAAS, especially the resulting increase of aldosterone may contribute to edema formation in COPD patients.
慢性阻塞性肺疾病(COPD)患者水肿的发病机制尚不清楚。在50例无肺心病的COPD患者中,我们测量了24小时水、钠和钾的排泄量、血浆中钠和钾的浓度以及肾素活性(PRA)、血管紧张素II(ATII)和醛固酮水平。我们发现,有水肿的COPD患者的PRA、ATII和醛固酮水平远高于无水肿患者,且水肿型COPD患者的钠和水排泄量显著减少。PRA、ATII和醛固酮升高与钠和水排泄能力下降相关。这些数据表明,除了高碳酸血症-低氧介导的肾功能紊乱外,肾素-血管紧张素-醛固酮系统(RAAS)的激活,尤其是由此导致的醛固酮增加,可能促使COPD患者形成水肿。