Creamer K M, McCloud L L, Fisher L E, Ehrhart I C
Department of Pediatrics, Section of Pediatric Critical Care Medicine, and Department of Physiology, Vascular Biology Center, Medical College of Georgia, Augusta, Georgia, USA.
Am J Respir Crit Care Med. 1998 Oct;158(4):1114-9. doi: 10.1164/ajrccm.158.4.9711081.
The aim of this study was to determine the relationship of pulmonary vascular resistance (PVR) hysteresis and lung volume, with special attention to the effects of ventilation around closing volume (CV). Isolated, blood-perfused canine left lower lung lobes (LLL) were incrementally inflated and deflated. Airway and pulmonary artery pressures (PAP) were recorded after each stepwise volume change. Constant blood flow was provided (600 ml/min) and the pulmonary vein pressure (PVP) was held constant at 5 cm H2O. PAP changes, therefore, were a direct index of PVR changes. Group 1 lobes underwent a full inflation from complete collapse to total lobe capacity (TLC) followed by a full deflation. Group 2 lobes underwent two deflation/inflation cycles, after an initial full inflation. These cycles, both beginning at TLC, had deflation end above and below CV, respectively. Significant PVR hysteresis was noted when the first inflation and deflation were compared. The maximum difference in PAP on deflation was 3.3 cm H2O or 11%. The mean decrease was 2.7 cm H2O for 18 lobes (p < 0.0001). The PAPs on all subsequent inflations or deflations that began above CV remained 9% lower than the initial inflation (n = 9, p < 0.0001), but were not different from each other. However, the final inflation which began from below CV resulted in a 30% return of PVR hysteresis (mean increase in PAP of 0.8 cm H2O, n = 7, p < 0.004). We conclude that there is hysteresis in the PVR response during ventilation, with decreased PVR during deflation relative to the initial inflation, that this hysteresis is absent when lung volume is maintained greater than CV, and that hysteresis returns when inflation occurs after deflation below CV.
本研究的目的是确定肺血管阻力(PVR)滞后与肺容积之间的关系,特别关注闭合容积(CV)附近通气的影响。对离体、血液灌注的犬左下肺叶(LLL)进行递增充气和放气。在每次逐步改变容积后记录气道和肺动脉压(PAP)。维持恒定的血流量(600 ml/min),并将肺静脉压(PVP)维持在5 cm H₂O 不变。因此,PAP 的变化是 PVR 变化的直接指标。第 1 组肺叶从完全萎陷完全充气至肺叶总容量(TLC),然后完全放气。第 2 组肺叶在初始完全充气后进行两个放气/充气循环。这两个循环均从 TLC 开始,放气终点分别在 CV 之上和之下。比较首次充气和放气时,观察到显著的 PVR 滞后。放气时 PAP 的最大差值为 3.3 cm H₂O 或 11%。18 个肺叶的平均下降值为 2.7 cm H₂O(p < 0.0001)。所有随后从 CV 之上开始的充气或放气时的 PAP 比初始充气时低 9%(n = 9,p < 0.0001),但彼此之间无差异。然而,从 CV 之下开始的最后一次充气导致 PVR 滞后恢复 30%(PAP 平均增加 0.8 cm H₂O,n = 7,p < 0.004)。我们得出结论,通气过程中 PVR 反应存在滞后现象,放气时 PVR 相对于初始充气时降低,当肺容积维持大于 CV 时这种滞后现象不存在,而当在 CV 之下放气后进行充气时滞后现象恢复。