LIMITATION TO EXERCISE AFTER PNEUMONECTOMY

肺切除术(PNX)为研究提供了强有力的实验工具 肺泡可量化损失的代偿性反应机制 毛细血管表面积，通风功率需求增加， 心脏和呼吸泵的不对称扭曲，并增加 肺血管阻力来自已知的血管床丢失。 机制包括毛细血管储备的补充，肺生长， 心脏和呼吸肌肥大。相对重要性和 这些机制的局限性尚不清楚。 在成年犬中，肺切除后的代偿性质和程度是 取决于切除的程度；相对补偿更多 58%的切除后较42%的切除后有活力。肺泡型肺生长 在58%切除后刺激，但在42%后不刺激。代偿性肺泡 生长并不伴随着呼吸道生长；呼吸道阻力和 左肺或左肺术后的通气量需求仍显著增加 右全肺切除术。横隔膜和横隔膜的解剖扭曲 肋间肌肉可能进一步导致呼吸紊乱 肌肉力学。我们的目标是定义限制和机制 犬广泛肺损伤后的功能损害及代偿 切除手术。我们问了以下几个问题：1)呼吸受限 显著导致术后最大吸氧量下降 全肺切除术？2)结构和功能的限制是什么？ 补偿？我们的假设是代偿性肺泡生长 在切除68%后会更有活力，但最终功能 容量将少于42%或58%的切除后的容量，因为 由于更广泛的呼吸道丢失而造成的更大的呼吸机功能障碍 横截面积，无代偿性呼吸道生长，和/或 呼吸泵的解剖扭曲。回答问题1 最大氧气摄取量将在没有外部负载的情况下测量，在外部负载下测量 负荷，使呼吸功增加2到3倍，并与系统 通过呼吸He-O2混合物来卸货。静态和动态测量 将测量肺和胸部的顺应性和阻力，以提供 呼吸总做功的估计值。呼吸肌血流量 运动中的需要量将由荧光素决定。 微球技术与通气量和血气测定同步进行 通风力。为了回答问题2，两阶段肺切除将 通过不平衡切除(右)切除68%的肺 PNX+左上肺叶切除术)导致纵隔移位和解剖 横隔肌和肋间肌扭曲，或由平衡引起 切除(每侧双叶切除)，每侧保留相同的肺体积 不伴纵隔移位和胸骨不对称扭曲的半胸 呼吸肌。对这些组的比较检查了 呼吸肌在固定扩张水平下的解剖扭曲 剩下的肺。补偿机制将从功能上进行研究 在清醒的狗的休息和锻炼以及安乐死后的结构上 肺和呼吸肌的形态计量学。

Pneumonectomy (PNX) provides a powerful experimental tool for studying mechanisms of compensatory response to quantifiable losses of alveolar capillary surface area, increased power requirements of ventilation, asymmetrical distortions of the heart and respiratory pumps, and increased pulmonary vascular resistance from a known loss of vascular bed. Mechanisms include recruitment of capillary reserves, lung growth, hypertrophy of heart and respiratory muscles. Relative importance and limits of these mechanisms are unclear. In adult dogs the nature and extent of compensation after pneumonectomy is dependent on the extent of resection; relative compensation is more vigorous after 58% resection than after 42%. Alveolar lung growth is stimulated after 58% resection but not after 42%. Compensatory alveolar growth is not accompanied by airway growth; airway resistance and ventilatory power requirements remain significantly elevated after left or right pneumonectomy. Anatomical distortion of the diaphragm and intercostal muscles may further contribute to derangement of respiratory muscle mechanics. Our objectives are to define the limits and mechanisms of functional impairment and compensation in dogs after extensive lung resection. We ask the following questions: 1) Do ventilatory limitations significantly contribute to the reduced maximal O2 uptake after pneumonectomy? 2) What are the limits of structural and functional compensation? Our hypothesis is that compensatory alveolar lung growth will be even more vigorous after 68% resection but ultimate functional capacity will be less than after either 42 or 58% resection because of greater ventilatory impairment owing to more extensive loss of airway cross-sectional area, the absence of compensatory airway growth, and/or anatomical distortion of the respiratory pump. To address Question 1 maximal O2 uptake will be measured with no external load, with external loads that increase work of breathing 2 to 3 fold and with the system unloaded by breathing a He-O2 mixture. Static and dynamic measurements of lung and thoracic compliance and resistance will be measured to provide estimates of total work of breathing. Respiratory muscle blood flow requirements during exercise will be determined by the fluorescent microsphere technique simultaneously with measurements of ventilation and ventilatory power. To address Question 2, two-stage lung resections will be performed, removing 68% of lung either by unbalanced resection (right PNX+left upper lobectomy) resulting in mediastinal shift and anatomical distortion of the diaphragm and intercostal muscles, or by balanced resection (bilobectomy on each side) leaving equal lung volumes in each hemithorax without mediastinal shift and asymmetrical distortion of respiratory muscles. Comparison of these groups examines the effects of anatomical respiratory muscle distortion at a fixed level of expansion of the remaining lung. Compensatory mechanisms will be studied functionally in the awake dog at rest and exercise and structurally after euthanasia by morphometry of both the lung and respiratory muscles.