PULMONARY LIMITATIONS TO EXERCISE AFTER PNEUMONECTOMY

在海平面上，正常人的运动限制是由 这些因素控制或决定最大心脏 产量及其分布。 可能除了 奥运级运动员的胸腔和肺泡泵功能 气体交换不会对运动施加重要限制， 然而，在高海拔的正常人中， 或在海平面有功能性肺损伤的患者中， 肺和胸腔可以对 运动能力 限制可能来自：1） 呼吸肌机械负荷增加; 2）受损 肺泡气体交换通过低O2扩散能力或低O2 驱动压力（高海拔）或区域匹配效率低， 通气和血液流动; 3）对 增加右心室后负荷的心血管功能， 夸大的机械心肺相互作用，例如，增加 肺和心窝僵硬，导致 舒张期充盈或来自肺的心脏降压反射。 这些潜在的运动来源的相对重要性 肺部疾病的局限性尚不清楚，难以接近 在人类身上进行实验。已经有许多动物模型 用于检查运动限制机制 心血管功能受损引起的，但实际上没有 检查受损肺的限制机制 功能 通过狗的肺切除术，我们可以增加 重复性方式的刚度和降低扩散能力 增加肺血管阻力。 这将 反过来增加呼吸功，减少肺泡储备 气体交换，增加右心室后负荷，也可能 减少心脏的前负荷。 在过去的31/2年里， 开发了技术来检查每一个潜在的 限制清醒犬运动的来源 侵入性方法和慢性器械的有限使用。 我们 计划是利用这些方法来表征性质， 运动限制的潜在来源的重要性 丧失肺实质的能力。

At sea level, exercise limitation in normal man is imposed by those factors which control or determine the maximal cardiac output and its distribution. With the possible exception of Olympic class athletes, pump function of the thorax and alveolar gas exchange do not impose an important limitation on exercise at sea level in normal man. However, in normal man at high altitude or in patients with functional lung impairment at sea level, the lungs and thorax can impose an important additional limitation on exercise capacity. Limitations potentially arise from: 1) increased mechanical load on respiratory muscles; 2) Impaired alveolar gas exchange by a low O2 diffusing capacity or low O2 driving pressure (high altitude) or inefficient regional matching of ventilation and blood flow; 3) Restrictions imposed on cardiovascular function by increased right ventricular afterload, exaggerated mechanical heart-lung interactions, e.g., increased stiffness of the lungs and cardiac fossa, causing impairment of diastolic filling or cardiodepressor reflexes from the lung. The relative importance of these potential sources of exercise limitation in lung disease are unclear and difficult to approach experimentally in man. There have been numerous animal models developed for examining mechanisms of exercise limitation caused by impaired cardiovascular function, but virtually none for examining mechanisms of limitation imposed by impaired lung function. By pneumonectomy in dogs, we can increase in a reproducible way the stiffness and reduce the diffusing capacity of the lungs and increase pulmonary vascular resistance. This will in turn increase work of breathing, reduce the reserve for alveolar gas exchange, increase right ventricular afterload, and may also reduce preload to the heart. Over the past 31/2 years we have developed the techniques to examine each of these potential sources of limitation to exercise in awake dogs using minimally invasive methods and limited use of chronic instrumentation. Our plan is to employ these methods to characterize the nature and importance of the potential sources of limitations in exercise capacity by loss of lung parenchyma.