急性肺损伤( ALI) 及急性呼吸窘迫综合征( ARDS) 是各种肺内外致病因素导致的急性呼吸衰竭, 以进行性呼吸困难和顽固性低氧血症为特征, 常继发于休克、创伤、严重感染以及大面积烧伤等疾病。病理以双肺弥漫性的渗出为特点。病情进展迅速, 预后极差, 具有很高死亡率。治疗时需要纠正缺氧, 以保证组织氧供。传统的常规机械通气( CMV) 在改善氧合、呼吸力学参数以及肺内炎症反应的同时, 导致肺损伤, 即呼吸机相关性肺损伤( VALI) 。近年认为, 采用高频振荡通气( HFOV) 代替CMV 能明显避免产生VALI, 并能改善ALI/ARDS的呼吸系统顺应性和氧合作用, 减轻肺内炎症反应和VALI, 利于急性损伤肺内塌陷和闭塞的小气道和肺泡重新开放。并且有人提出HFOV 与部分液体通气( PLV)联用( HFOV-PLV) 可进一步改善气体交换, 抑制肺组织的炎性反应, 减少肺损伤及氟碳化合物( PFCs) 用量, 稳定全身血液循环, 减少中枢神经系统( CNS) 并发症[ 1] 。
Objective To investigate the effect of partial liquid ventilation (PLV) with perfluorocarbon(PFC) and continuous pulmonary artery perfusion (CPP) on lung gas exchange and lung inflammatory reaction in acute lung injury(ALI) induced by cardiopulmonary bypass (CPB). Methods Eighteen of either sex piglets(weighting10.2±1.6kg) were randomly divided into three groups: Control group, CPP+CPB group (CPP group), PLV+CPP+CPB group (PLV group). Animals in control group received no treatment but conventional mechanical ventilation.In CPP group lung perfusion with oxygenated blood at 20-25ml/kg·min was given during aortic clamping. In PLV group PFC (FDC)12ml/kg was instilled into the trachea right after CPB stopping. The changes of gas exchange were mearsured before CPB and at 0h, 1h, 2h, 3h after CPB stopping. Histological sections were taken from right and left downsides of lung. Results Compared with control group, the partial pressure of oxygen in artery (PaO2) significantly increased and alveolar-aterial oxygen gradient(AaDO2) markedly decreased after 1h in PLV group(Plt;005) and partial pressure of carbon dioxide in artery (PaCO2) also became small after 3h (Plt;005).The change of gas exchange in CPP group was markedly improved. And role of lung protection of PLV was more better than that of CPP. Light microscopy: Express of intercellular adhesion molecule-1(ICAM-1) in the histopathological lesions of lung was bely positive in control group than that of PLV group and CPP group. Conclusion PLV and continuous pulmonary artery perfusion can improve the oxygenation of lung and inhibit inflammatory reaction of acute lung injury induced by CPB