1Department of Pediatric Intensive Care, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, The Netherlands. 2Department of Pediatric Infectious Diseases, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, The Netherlands.
Pediatr Crit Care Med. 2014 Jan;15(1):e27-31. doi: 10.1097/01.pcc.0000436197.07713.30.
Respiratory syncytial virus lower respiratory tract infection is the most frequent cause of respiratory insufficiency necessitating mechanical ventilation in infants during the winter season. Recently, we presented a new animal model to show that mechanical ventilation aggravates respiratory syncytial virus-induced pulmonary inflammation by distinct mechanisms. We now use this model to study whether low tidal volume mechanical ventilation causes less ventilator-induced lung injury in the presence of respiratory syncytial virus lower respiratory tract infection.
Randomized controlled experimental study.
University Medical Center animal laboratory.
Male BALB/c mice, 6-8 weeks old and weighing 20-28 g.
Mice were inoculated with respiratory syncytial virus or mock virus on day 0 and ventilated on day 1 or 5 with high (12 mL/kg) or low (6 mL/kg) tidal volume for 5 hours.
Total and differential cell counts as well as cytokine concentrations were determined in bronchoalveolar lavage fluid. Compared with nonventilated respiratory syncytial virus-infected mice, high tidal volume ventilation of respiratory syncytial virus-infected mice on day 5 enhanced bronchoalveolar lavage fluid total cell count (0.35 vs 0.99 × 10e6/mL; p < 0.01), neutrophils (0.02 vs 0.17 × 10e6/mL; p < 0.01), interleukin-6 (58 vs 250 pg/mL; p < 0.01), and keratinocyte-derived chemokine (95 vs 335 pg/mL; p < 0.01) levels. In low tidal volume ventilation of respiratory syncytial virus-infected mice, no significant difference in cell counts or cytokine concentrations was observed compared with spontaneous breathing respiratory syncytial virus-infected controls on both days.
Low tidal volume mechanical ventilation causes less ventilation-induced cellular and cytokine influx into the bronchoalveolar space during respiratory syncytial virus lower respiratory tract infection.
呼吸道合胞病毒下呼吸道感染是导致婴儿在冬季需要机械通气以缓解呼吸功能不全的最常见原因。最近，我们提出了一种新的动物模型，表明机械通气通过不同的机制加重呼吸道合胞病毒引起的肺部炎症。现在，我们使用该模型研究在呼吸道合胞病毒下呼吸道感染的情况下，小潮气量机械通气是否会导致较少的呼吸机相关性肺损伤。
随机对照实验研究。
大学医学中心动物实验室。
6-8 周龄、体重 20-28g 的雄性 BALB/c 小鼠。
小鼠于第 0 天接种呼吸道合胞病毒或模拟病毒，于第 1 天或第 5 天以高（12ml/kg）或低（6ml/kg）潮气量进行 5 小时机械通气。
通过支气管肺泡灌洗（BAL）液测定总细胞计数和分类计数以及细胞因子浓度。与未通气的呼吸道合胞病毒感染小鼠相比，第 5 天高潮气量通气的呼吸道合胞病毒感染小鼠的 BAL 液总细胞计数（0.35 对 0.99×10e6/ml；p<0.01）、中性粒细胞（0.02 对 0.17×10e6/ml；p<0.01）、白细胞介素-6（58 对 250pg/ml；p<0.01）和角质细胞衍生的趋化因子（95 对 335pg/ml；p<0.01）水平均增加。在低潮气量通气的呼吸道合胞病毒感染小鼠中，与第 5 天自发呼吸的呼吸道合胞病毒感染对照组相比，细胞计数或细胞因子浓度无显著差异。
在呼吸道合胞病毒下呼吸道感染期间，小潮气量机械通气导致进入支气管肺泡腔的通气诱导细胞和细胞因子的量减少。
