Institute of Clinical Physiology, Pisa, Italy.
Department of Cardiology, University Hospital of Bern, Bern, Switzerland; Department of Internal Medicine and Botnar Center for Clinical Research, Lausanne, Switzerland.
Chest. 2012 Apr;141(4):953-958. doi: 10.1378/chest.11-0084. Epub 2011 Sep 1.
Chronic mountain sickness (CMS) is a major public health problem in mountainous regions of the world. In its more advanced stages, exercise intolerance is often found, but the underlying mechanism is not known. Recent evidence indicates that exercise-induced pulmonary hypertension is markedly exaggerated in CMS. We speculated that this problem may cause pulmonary fluid accumulation and aggravate hypoxemia during exercise.
We assessed extravascular lung water (chest ultrasonography), pulmonary artery pressure, and left ventricular function in 15 patients with CMS and 20 control subjects at rest and during exercise at 3,600 m.
Exercise at high altitude rapidly induced pulmonary interstitial fluid accumulation in all patients but one (14 of 15) with CMS and further aggravated the preexisting hypoxemia. In contrast, in healthy high-altitude dwellers exercise did not induce fluid accumulation in the majority of subjects (16 of 20) (P = .002 vs CMS) and did not alter arterial oxygenation. Exercise-induced pulmonary interstitial fluid accumulation and hypoxemia in patients with CMS was accompanied by a more than two times larger increase of pulmonary artery pressure than in control subjects (P < .001), but no evidence of left ventricular dysfunction. Oxygen inhalation markedly attenuated the exercise-induced pulmonary hypertension (P < .01) and interstitial fluid accumulation (P < .05) in patients with CMS but had no detectable effects in control subjects.
To our knowledge, these findings provide the first direct evidence that exercise induces rapid interstitial lung fluid accumulation and hypoxemia in patients with CMS that appear to be related to exaggerated pulmonary hypertension. We suggest that this problem contributes to exercise intolerance in patients with CMS.
ClinicalTrials.gov; No.: NCT01182792; URL: www.clinicaltrials.gov.
慢性山病（CMS）是世界山区的一个主要公共卫生问题。在其更晚期阶段，通常会发现运动不耐受，但潜在机制尚不清楚。最近的证据表明，CMS 患者运动引起的肺动脉高压明显加剧。我们推测这个问题可能导致运动时肺部液体蓄积并加重低氧血症。
我们评估了 15 名 CMS 患者和 20 名对照者在休息和 3600 米运动时的肺血管外肺水（胸部超声）、肺动脉压和左心室功能。
在 CMS 患者中，高海拔运动迅速导致所有患者（15 例中的 14 例）肺部间质液蓄积，并进一步加重了先前存在的低氧血症。相比之下，在健康的高原居民中，运动在大多数受试者中（20 例中的 16 例）没有引起液体蓄积（P =.002 与 CMS 相比），也没有改变动脉氧合。CMS 患者运动引起的间质液蓄积和低氧血症伴随着肺动脉压增加两倍以上，而对照组没有（P <.001），但没有左心室功能障碍的证据。吸氧显著减轻 CMS 患者运动引起的肺动脉高压（P <.01）和间质液蓄积（P <.05），但对对照组没有可检测到的影响。
据我们所知，这些发现首次提供了直接证据，表明运动在 CMS 患者中迅速引起间质肺液蓄积和低氧血症，这似乎与肺动脉高压加剧有关。我们认为，这个问题导致 CMS 患者运动不耐受。
ClinicalTrials.gov；编号：NCT01182792；网址：www.clinicaltrials.gov。
