Stewart A G, Waterhouse J C, Billings C G, Baylis P, Howard P
Department of Medicine and Pharmacology, Royal Hallamshire Hospital, Sheffield, UK.
Thorax. 1994 Oct;49(10):995-8. doi: 10.1136/thx.49.10.995.
Some patients with hypoxaemic chronic obstructive pulmonary disease (COPD) develop cor pulmonale with sodium and water retention. The sodium retention has been explained as a result of increased plasma levels of aldosterone. If this was true angiotensin converting enzyme (ACE) inhibition would be expected to lower plasma levels of aldosterone and improve the renal excretion of sodium.
Six patients with stable hypoxaemic COPD (PaO2 < 8.0 kPa) and a history of an oedematous exacerbation received an intravenous hypertonic saline load (6 ml/kg body weight of 2.7% saline over one hour) before and while taking 4 mg/day perindopril, an ACE inhibitor, for one month. Aldosterone, antidiuretic hormone (ADH), plasma and urine electrolyte levels, osmolality, and volume were measured over four hours. The repeatability of the saline load test was assessed in six patients with a similar severity of hypoxaemic COPD. For comparison the saline load test was also performed in six patients with mild COPD.
The hypertonic saline load test results were repeatable. Perindopril reduced the mean (SD) plasma level of aldosterone from 142 (88) pg/ml to 54 (24) pg/ml at 0 minutes before the saline infusion, and from 64 (35) pg/ml to 30 (17) pg/ml after the infusion without improving the urinary volume or sodium excretion. Before starting treatment with perindopril 43.7 (6.9) mmol (20%) of the sodium load was excreted compared with 49.6 (7.9) mmol (22% of load) when taking perindopril. Patients with mild COPD excreted more sodium (77.6 (21.4) mmol (38.7% of load)) despite having similar plasma aldosterone levels to those in the patients receiving perindopril.
Patients with stable hypoxaemic COPD have an impaired ability to excrete sodium which is not improved by the administration of an ACE inhibitor. ACE inhibition lowered the plasma level of aldosterone without improving sodium excretion. This suggests that the inability of patients with hypoxaemic COPD to excrete sodium is not caused by their increased plasma levels of aldosterone.
一些低氧性慢性阻塞性肺疾病（COPD）患者会出现肺心病并伴有钠水潴留。钠潴留被解释为醛固酮血浆水平升高的结果。如果真是这样，那么血管紧张素转换酶（ACE）抑制作用有望降低醛固酮的血浆水平并改善肾脏对钠的排泄。
6例病情稳定的低氧性COPD患者（动脉血氧分压<8.0kPa）且有水肿加重病史，在服用4mg/天培哚普利（一种ACE抑制剂）一个月之前及服药期间，接受静脉输注高渗盐水负荷试验（1小时内输注6ml/kg体重的2.7%盐水）。在4小时内测量醛固酮、抗利尿激素（ADH）、血浆及尿液电解质水平、渗透压和容量。在6例低氧性COPD严重程度相似的患者中评估盐水负荷试验的可重复性。为作比较，也在6例轻度COPD患者中进行了盐水负荷试验。
高渗盐水负荷试验结果具有可重复性。培哚普利使输注盐水前0分钟时醛固酮的平均（标准差）血浆水平从142（88）pg/ml降至54（24）pg/ml，输注后从64（35）pg/ml降至30（17）pg/ml，但未改善尿量或钠排泄。在开始使用培哚普利治疗前，钠负荷的43.7（6.9）mmol（20%）被排泄，而服用培哚普利时为49.6（7.9）mmol（负荷的22%）。轻度COPD患者排泄更多的钠（77.6（21.4）mmol（负荷的38.7%）），尽管其血浆醛固酮水平与接受培哚普利治疗的患者相似。
病情稳定的低氧性COPD患者排泄钠的能力受损，给予ACE抑制剂并不能改善这一情况。ACE抑制作用降低了醛固酮的血浆水平，但未改善钠排泄。这表明低氧性COPD患者不能排泄钠并非由其血浆醛固酮水平升高所致。
