Objective: 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.
Design: Randomized controlled experimental study.
Setting: University Medical Center animal laboratory.
Subjects: Male BALB/c mice, 6–8 weeks old and weighing 20–28 g.
Interventions: 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.
Measurements and Main Results: 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.
Conclusions: 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.
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.
Supported, in part, by two European Society of Pediatric Infectious Diseases (ESPID) Small Grant Awards.
The authors have disclosed that they do not have any potential conflicts of interest.
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