Stewart A G, Waterhouse J C, Billings C G, Baylis P H, Howard P
Department of Medicine and Pharmacology, Royal Hallamshire Hospital, Sheffield, UK.
Thorax. 1995 Aug;50(8):838-45. doi: 10.1136/thx.50.8.838.
Some patients with hypoxaemic chronic obstructive pulmonary disease (COPD) develop sodium and water retention and a subclinical autonomic neuropathy. The possibility that these might be associated has been investigated.
The ability of 24 patients with COPD to excrete a 6 ml/kg 2.7% intravenous saline or 15 ml/kg oral water load was studied and changes in plasma electrolyte levels, osmolality, plasma aldosterone and vasopressin levels, urinary volume and sodium content, glomerular filtration rate, renal blood flow, and cardiovascular autonomic nerve function were measured. Patients were divided into groups of eight: those in group A (controls) had mild COPD with a Pa02 of > 9 kPa and no oedema, patients in group B were more hypoxaemic but had never been oedematous, whilst those in group C were hypoxaemic and mildly oedematous at the time of the study.
Patients in groups B and C excreted less sodium and water during saline loading and a lesser proportion of the water load. Patients in group C had a reduction in renal blood flow and glomerular filtration rate and all had a subclinical autonomic neuropathy, which was also found in three patients in group B. Their plasma aldosterone level was raised but did suppress appropriately on saline loading. Vasopressin levels were abnormally raised for the osmolality in patients in group C and in those with autonomic dysfunction throughout the water load and at 240 minutes after the salt load. Sodium and urine excretion was highly correlated with autonomic dysfunction, aldosterone levels at time zero, and renal blood flow. The 11 patients with autonomic dysfunction were more likely to be oedematous, more hypoxaemic, excreted much less urine and sodium, had lower glomerular filtration rate and renal blood flow, and higher aldosterone and vasopressin levels than the remaining patients.
In patients with COPD the inability to excrete sodium and water is multifactorial. This is the first study to show that autonomic dysfunction is at least associated and might play an important part in the impaired sodium and water homeostasis seen in patients with severe COPD.
一些低氧性慢性阻塞性肺疾病（COPD）患者会出现钠水潴留和亚临床自主神经病变。已经对二者可能存在关联的可能性进行了研究。
研究了24例COPD患者排泄6 ml/kg 2.7%静脉生理盐水或15 ml/kg口服水负荷的能力，并测量了血浆电解质水平、渗透压、血浆醛固酮和血管加压素水平、尿量和钠含量、肾小球滤过率、肾血流量以及心血管自主神经功能。患者被分为八组：A组（对照组）为轻度COPD患者，动脉血氧分压（PaO₂）> 9 kPa且无水肿；B组患者缺氧程度更重，但从未出现过水肿；而C组患者在研究时处于缺氧且轻度水肿状态。
B组和C组患者在静脉输注生理盐水期间排泄的钠和水较少，口服水负荷后排出的水比例也较低。C组患者肾血流量和肾小球滤过率降低，且均有亚临床自主神经病变，B组的3例患者也有此病变。他们的血浆醛固酮水平升高，但在静脉输注生理盐水后能适当抑制。C组患者以及在整个水负荷期间和盐负荷后240分钟时出现自主神经功能障碍的患者，其血管加压素水平相对于渗透压异常升高。钠和尿排泄与自主神经功能障碍、零时醛固酮水平以及肾血流量高度相关。与其余患者相比，11例有自主神经功能障碍的患者更易出现水肿、缺氧程度更重、尿和钠排泄量少得多、肾小球滤过率和肾血流量更低，醛固酮和血管加压素水平更高。
COPD患者排钠排水能力不足是多因素导致的。这是第一项表明自主神经功能障碍至少与之相关且可能在重度COPD患者钠水平衡受损中起重要作用的研究。
