机械通气动态通气参数对急性呼吸窘迫综合征犬肺损伤的影响

目的观察机械通气动态通气参数对急性呼吸窘迫综合征(ARDS)犬肺损伤的影响,评价机械通气参数对肺损伤的保护作用。方法36条健康杂种犬,按照随机数字表法分为正常对照组(N组)、模型组(M组)及机械通气A～D组。采用气管内盐酸吸入法建立ARDS模型,按下述方案机械通气。A组:小潮气量(6ml/kg)、低吸气流速(6ml·kg-1·s-1)、高通气频率(30次/min);B组:大潮气量(20ml/kg)、高吸气流速(20ml·kg-1·s-1)、高通气频率(30次/min);C组:大潮气量(20ml/kg)、高吸气流速(17ml·kg-1·s-1)、低通气频率(15次/min);D组:大潮气量(20ml/kg)、低吸气流速(10ml·kg-1·s-1)、低通气频率(15次/min)。分组机械通气后0、1、2和4h各时间点分别记录呼吸力学各值。4h后处死动物,取肺脏测肺湿/干重(W/D)比值;光镜下观察病理组织学变化,并进行弥漫性肺泡损伤(DAD)评分及高倍镜下中性粒细胞计数;流式细胞仪检测肺组织核转录因子κB(NFκB)p65活性。结果B组肺W/D比值为9.95±0.99,高于A组6.78±0.56、D组7.11±0.47(P均<0.01),但与C组9.22±1.19差别不大(P>0.05)。肺组织病理DAD评分:B组为(12.80±1.47)分,明显高于A组(7.67±1.20)分和D组(8.83±1.17)分(P均<0.01),但与C组(11.50±1.87)分比较差异无显著性(P>0.05)。B组NFκBp65表达为(33.56±2.85)%,较A、D两组〔(10.35±0.60)%、(10.79±1.02)%〕表达增强(P均<0.01),与C组(30.87±1.16)%间比较差异无显著性(P>0.05)。结论大潮气量、高吸气流速、高通气频率机械通气可导致严重的呼吸机相关性肺损伤(VILI),降低通气频率可适当减轻这类损伤;在大潮气量基础上,降低通气频率及吸气流速,对损伤的肺组织可起到一定的保护作用。

Effects of different modes of artificial ventilation on lung injury in dog model of acute respiratory distress syndrome

OBJECTIVE: To investigate the effects of different modes of artificial ventilation on lung injury in a dog model of acute respiratory distress syndrome (ARDS), and to evaluate the protective effect of various parameters in mechanical ventilation on lung injury. METHODS: Thirty-six healthy dogs were randomly divided into normal control group (N group), ARDS group (M group) and ventilation group (A-D groups) based on a series of random number. The ARDS dog model was replicated by intratracheal instillation of hydrochloric acid, and mechanical ventilation was carried out according to the following ventilatory protocols. A group: low V(T) (6 ml/kg) with respiratory rate 30/minutes, low inspiratory flow 6 ml.kg(-1).s(-1). B group: large V(T) (20 ml/kg) with respiratory rate 30/minutes, high inspiratory flow 20 ml.kg(-1).s(-1). C group: large V(T) (20 ml/kg) with respiratory rate 15/minutes, high inspiratory flow 17 ml.kg(-1).s(-1). D group: large V(T) (20 ml/kg) with respiratory rate 15/minutes, low inspiratory flow 10 ml.kg(-1).s(-1). Lung mechanical parameters were recorded at 0, 1, 2 and 4 hours after the change in ventilatory protocol. After 4 hours of mechanical ventilation, animals were sacrificed, and the lung was harvested. Lung wet/dry weight ratio (W/D) was measured. Histopathological changes were observed under light microscope, diffuse alveolar damage (DAD) scores was estimated, and polymorphonuclear leucocytes (PMN) count was done. Nuclear factor-KappaB (NF-KappaB) p65 activity was assessed by flow cytometry. RESULTS: W/D in B group (9.95+/-0.99) was higher than that of A (6.78+/-0.56) and D (7.11+/-0.47) groups (both P<0.01),but there was no significant difference between B and C groups (9.22+/-1.19, P>0.05). DAD scores in B group (12.80+/-1.47) was obvious higher than that of A (7.67+/-1.20) and D (8.83+/-1.17) groups (both P<0.01), but there was no difference compared with C group (11.50+/-1.87, P>0.05). NF-KappaB p65 activity in B group [(33.56+/-2.85)%] was significantly higher than that of A [(10.35+/-0.60)%] and D [(10.79+/-1.02)%] groups, but there was no difference between B and C [(30.87+/-1.16)%] groups. CONCLUSION: Large tidal volumes with high inspiratory flow and high respiratory rate may cause severe ventilator induced lung injury (VILI). Reduction of inspiratory flow and respiratory rate with large tidal volume ventilation may provide pulmonary protection.