Center for Pulmonary Vascular Disease, Division of Cardiology, Azrieli Heart Center, and Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
Pulmonary Hypertension Clinic, Attikon Hospital, and 2nd Department of Critical Care, National and Kapodistrian University of Athens, Athens, Greece.
Am J Physiol Lung Cell Mol Physiol. 2019 Sep 1;317(3):L361-L368. doi: 10.1152/ajplung.00098.2019. Epub 2019 Jun 26.
In exercising humans, cardiac output (CO) increases, with minor increases in pulmonary artery pressure (PAP). It is unknown if the CO is accommodated via distention of already perfused capillaries or via recruitment of nonconcomitantly perfused pulmonary capillaries. Ten subjects (9 female) performed symptom-limited exercise. Six had resting mean PAP (PAPm) <20 mmHg, and four had PAPm between 21 and 24 mmHg. The first-pass pulmonary circulatory metabolism of [H]benzoyl-Phe-Ala-Pro (BPAP) was measured at rest and at peak exercise, and functional capillary surface area (FCSA) was calculated. Data are means ± SD. Mean pulmonary arterial pressure rose from 18.8 ± 3.3 SD mmHg to 28.5 ± 4.6 SD mmHg, CO from 6.4 ± 1.6 to 13.4 ± 2.9 L/min, and pulmonary artery wedge pressure from 14 ± 3.3 to 19.5 ± 5 mmHg (all ≤ 0.001). Percent BPAP metabolism fell from 74.7 ± 0.1% to 67.1 ± 0.1%, and FCSA/body surface area (BSA) rose from 2,939 ± 640 to 5,018 ± 1,032 mL·min·m (all < 0.001). In nine subjects, the FCSA/BSA-to-CO relationship suggested principally capillary recruitment and not distention. In , a marathon runner, resting CO and FCSA/BSA were high, and increases with exercise suggested distention. Exercising humans demonstrate pulmonary capillary recruitment and distention. At moderate resting CO, increasing blood flow causes principally recruitment while, based on one subject, when exercise begins at high CO, further increases appear to cause distention. Our findings clarify an important physiologic question. The technique may provide a means for further understanding exercise physiology, its limitation in pulmonary hypertension, and responses to therapy.
在人体运动中，心输出量（CO）增加，肺动脉压（PAP）略有增加。目前尚不清楚 CO 是通过已经灌注的毛细血管扩张来适应，还是通过募集非同时灌注的肺毛细血管来适应。10 名受试者（9 名女性）进行了症状限制运动。6 名受试者静息平均肺动脉压（PAPm）<20mmHg，4 名受试者 PAPm 在 21-24mmHg 之间。在休息和运动峰值时测量了 [H]苯甲酰-Phe-Ala-Pro（BPAP）的第一通过肺循环代谢，并计算了功能毛细血管表面积（FCSA）。数据为平均值±标准差。平均肺动脉压从 18.8±3.3SDmmHg 升高至 28.5±4.6SDmmHg，CO 从 6.4±1.6L/min 升高至 13.4±2.9L/min，肺动脉楔压从 14±3.3mmHg 升高至 19.5±5mmHg（均 ≤ 0.001）。BPAP 代谢百分比从 74.7±0.1%下降至 67.1±0.1%，FCSA/体表面积（BSA）从 2939±640mL·min·m 升高至 5018±1032mL·min·m（均 < 0.001）。在 9 名受试者中，FCSA/BSA 与 CO 的关系提示主要是毛细血管募集，而不是扩张。在 1 名马拉松跑者中，静息 CO 和 FCSA/BSA 较高，运动时的增加提示扩张。运动中的人体表现出肺毛细血管募集和扩张。在中等静息 CO 时，增加血流量主要引起募集，而基于 1 名受试者，当运动开始时 CO 较高时，进一步的增加似乎会引起扩张。我们的发现澄清了一个重要的生理问题。该技术可能为进一步了解运动生理学、其在肺动脉高压中的局限性以及对治疗的反应提供一种手段。
