Dane D Merrill, Yilmaz Cuneyt, Gyawali Dipendra, Iyer Roshni, Ravikumar Priya, Estrera Aaron S, Hsia Connie C W
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; and.
Department of Cardiothoracic Surgery, University of Texas Southwestern Medical Center, Dallas, Texas.
J Appl Physiol (1985). 2016 Jul 1;121(1):312-23. doi: 10.1152/japplphysiol.00297.2016. Epub 2016 May 5.
Following pneumonectomy (PNX), two separate mechanical forces act on the remaining lung: parenchymal stress caused by lung expansion, and microvascular distension and shear caused by increased perfusion. We previously showed that parenchymal stress and strain explain approximately one-half of overall compensation; the remainder was presumptively attributed to perfusion-related factors. In this study, we directly tested the hypothesis that perturbation of regional pulmonary perfusion modulates post-PNX lung growth. Adult canines underwent banding of the pulmonary artery (PAB) to the left caudal (LCa) lobe, which caused a reduction in basal perfusion to LCa lobe without preventing the subsequent increase in its perfusion following right PNX while simultaneously exaggerating the post-PNX increase in perfusion to the unbanded lobes, thereby creating differential perfusion changes between banded and unbanded lobes. Control animals underwent sham pulmonary artery banding followed by right PNX. Pulmonary function, regional pulmonary perfusion, and high-resolution computed tomography of the chest were analyzed pre-PNX and 3-mo post-PNX. Terminally, the remaining lobes were fixed for detailed morphometric analysis. Results were compared with corresponding lobes in two control (Sham banding and normal unoperated) groups. PAB impaired the indices of post-PNX extravascular alveolar tissue growth by up to 50% in all remaining lobes. PAB enhanced the expected post-PNX increase in alveolar capillary formation, measured by the prevalence of double-capillary profiles, in both unbanded and banded lobes. We conclude that perfusion distribution provides major stimuli for post-PNX compensatory lung growth independent of the stimuli provided by lung expansion and parenchymal stress and strain.
肺切除术后，两种不同的机械力作用于剩余肺组织：肺扩张引起的实质应力，以及灌注增加导致的微血管扩张和剪切力。我们之前的研究表明，实质应力和应变约占总体代偿的一半；其余部分推测归因于与灌注相关的因素。在本研究中，我们直接检验了以下假设：局部肺灌注的扰动调节肺切除术后肺的生长。成年犬接受肺动脉（PAB）至左尾叶（LCa）的结扎，这导致LCa叶基础灌注减少，同时不阻止右肺切除术后其灌注的随后增加，而同时夸大了肺切除术后未结扎叶灌注的增加，从而在结扎叶和未结扎叶之间产生不同的灌注变化。对照动物接受假肺动脉结扎，随后进行右肺切除术。在肺切除术前和术后3个月分析肺功能、局部肺灌注和胸部高分辨率计算机断层扫描。最后，将剩余叶固定以进行详细的形态计量分析。将结果与两个对照组（假结扎和正常未手术）的相应叶进行比较。PAB使所有剩余叶肺切除术后血管外肺泡组织生长指数受损高达50%。PAB增强了肺切除术后肺泡毛细血管形成的预期增加，通过双毛细血管轮廓的发生率来衡量，在未结扎叶和结扎叶中均如此。我们得出结论，灌注分布为肺切除术后代偿性肺生长提供了主要刺激，独立于肺扩张以及实质应力和应变所提供的刺激。
