高容量血液滤过对内毒素诱导急性肺损伤犬肺表面活性蛋白的影响

目的观察高容量血液滤过（HVHF）对内毒素诱导急性肺损伤（ALI）犬肺表面活性蛋白（SP）的影响。方法采用中心静脉注入脂多糖（LPS）制备犬ALI模型。随机将16条健康犬分为两组，模型组动物制模后采用单纯机械通气治疗；治疗组制模后采用机械通气＋HVHF治疗。监测两组动物基础值、成模时以及HVHF治疗1、2和4h的动脉血气及呼吸力学指标变化。采用蛋白质免疫印迹法（Western blot）测定肺组织匀浆内SP—B含量的变化。结果注入LPS后动物动脉血氧分压（PaO2）和氧合指数（PaO2／FiO2）均下降（P均＜0．05），成模时PaO2／FiO2＜300mmHg（1mmHg：0．133kPa）；HVHF治疗后4hPaO2、Pa02／FiO2均明显高于模型组（P均＜0．01）。模型组动物治疗后吸气阻力（Raw）、气道峰压（PIP）均保持稳定，治疗4h时肺动态顺应性（Cdyn）、肺总顺应性（Ctot）均下降，呼吸功（WOBvent）上升（P均＜0．01）；HVHF治疗后各指标均保持稳定，治疗4h后Cdyn和Ctot均较模型组差异有显著性（P＜0．01和P＜0．05）。治疗组肺组织匀浆SP—B的含量明显高于模型组（P＜0．01）。结论HVHF能有效地提高ALI犬肺组织SP—B的含量，达到阻止ALI呼吸力学恶化、改善氧合的目的。

Effect of high volume hemofiltration on pulmonary surfactant protein in endotoxin induced acute lung injury in dog

OBJECTIVE: To explore the effect of high volume hemofiltration (HVHF) on pulmonary surfactant protein (SP) in endotoxin induced acute lung injury (ALI) in dogs. METHODS: Sixteen healthy male mongrel dogs were given lipopolysaccharide(LPS 650 mug/kg) via central vein within 30 minutes. After the reproduction of the model, they were divided into two groups randomly (n=8). One group received the treatment of HVHF and mechanical ventilation (MV, treatment group), while another received only MV (model group). Parameters of arterial blood gas and respiratory mechanics were recorded at basic values, after reproduction of the experimental model, and 1, 2 and 4 hours after HVHF. Content of SP-B in lung tissue homogenate was measured by protein Western blot. RESULTS: After injection of LPS, partial pressure of oxygen in artery (PaO(2)) and PaO(2)/fractional concentration of inspired oxygen (FiO(2)) began to decrease (both P<0.05). PaO(2)/FiO(2) <300 mm Hg (1 mm Hg=0.133 kPa) when ALI was reproduced. PaO(2) and PaO(2)/FiO(2) were higher in treatment group than those in model group 4 hours after HVHF (both P<0.01). Inspiratory resistance of airway (Raw) and peak inspiratory pressure (PIP) in model group were kept stable after MV. Lung dynamic compliance (Cdyn) and lung total compliance (Ctot) in model group were both decreased while ventilatory work of breathing (WOBvent) increased 4 hours after MV (all P<0.01). All parameters in the treatment group were kept stable and differences in Cdyn and Ctot were significant at 4 hours after HVHF compared to model group (P<0.01 and P<0.05). Content of SP-B in lung tissue homogenate was significantly higher in treatment group than that in model group (P<0.01). CONCLUSION: HVHF could effectively increase the content of SP-B in lung to prevent aggravation of respiratory mechanics and improve oxygenation.