DeCampos K N, Keshavjee S, Slutsky A S, Liu M
Division of Thoracic Surgery, The Toronto Hospital, Ontario, Canada.
J Heart Lung Transplant. 1999 Nov;18(11):1096-102. doi: 10.1016/s1053-2498(99)00082-0.
Physical factors play an important role in ischemia-reperfusion-induced injury of lung transplants. For example, rapid restoration of reperfusion resulted in severe pulmonary edema and deterioration of pulmonary function of lung explants in an ex vivo reperfusion system. This type of injury can be prevented by a stepwise increase in the perfusion flow rate, or by adding prostaglandin E1 (PGE1) to the blood perfusate during the first 10 minutes. However, the mechanisms of these protective effects are unknown. We noted a dramatic decrease in airway pressure rather than pulmonary arterial pressure in these studies, suggesting that lung recruitment may be an important factor in minimizing injury.
In the present study, we examined the importance of alveolar recruitment in preventing rapid-reperfusion-induced lung injury. Rat lungs were flushed preserved with low potassium dextran solution for 12 hours at 4 degrees C. Lung explants were randomly divided into three groups: 1) untreated control; 2) lungs inflated to total lung capacity for 2 minutes; and 3) lungs ventilated for 10 minutes prior to reperfusion. Postpreservation lung function was assessed in an isolated rat lung reperfusion model.
Rapid initiation of reperfusion led to severe pulmonary edema and significant pulmonary dysfunction. In inflation or ventilation groups, the injury was significantly attenuated. The PaO2 and shunt fractions in these lungs were comparable to normal lungs. A significant drop in airway pressure was observed in these two groups and the lung compliance in the inflation group was significantly better than other two groups.
These results suggest that overcoming alveolar collapse with inflation or ventilation, may protect the lung from mechanical-stress-induced injury during reperfusion.
物理因素在肺移植缺血再灌注损伤中起重要作用。例如，在体外再灌注系统中，快速恢复再灌注会导致严重肺水肿和肺外植体肺功能恶化。这种损伤可通过逐步增加灌注流速或在最初10分钟内向血液灌注液中添加前列腺素E1（PGE1）来预防。然而，这些保护作用的机制尚不清楚。我们在这些研究中注意到气道压力而非肺动脉压力急剧下降，这表明肺复张可能是将损伤降至最低的一个重要因素。
在本研究中，我们研究了肺泡复张在预防快速再灌注诱导的肺损伤中的重要性。大鼠肺用低钾右旋糖酐溶液在4℃冲洗保存12小时。肺外植体随机分为三组：1）未处理对照组；2）肺充气至肺总量2分钟；3）再灌注前通气10分钟。在离体大鼠肺再灌注模型中评估保存后肺功能。
快速开始再灌注导致严重肺水肿和明显的肺功能障碍。在充气或通气组中，损伤明显减轻。这些肺中的动脉血氧分压（PaO2）和分流分数与正常肺相当。在这两组中观察到气道压力显著下降，并且充气组的肺顺应性明显优于其他两组。
这些结果表明，通过充气或通气克服肺泡萎陷，可能在再灌注期间保护肺免受机械应力诱导的损伤。
