Abstract

Mechanical ventilation (MV) may amplify the lung-specific inflammatory response in preinjured lungs by elevating cytokine release and augmenting damage to the alveolar integrity. In this study, we test the hypothesis that MV exerts different negative impacts on inflammatory response at different time points of postlung injury. Basic lung injury was induced by cecal ligation and puncture (CLP) surgery in rats. Physiological indexes including blood gases were monitored during MV and samples were assessed following each experiment. Low V T (tidal volume) MV caused a slight increase in cytokine release and tissue damage at day 1 and day 4 after sepsis induced lung injury, while cytokine release from the lungs in the two moderately ventilated V T groups was amplified. Interestingly, in the two groups where rats received low V T MV, we found that infiltration of inflammatory cells was only profound at day 4 after CLP. Marked elevation of protein leakage indicated a compromise in alveolar integrity in rats that received moderate V T MV at day 4 following CLP, correlating with architectural damage to the alveoli. Our study indicates that preinjured lungs are more sensitive to mechanical MV at later phases of sepsis, and this situation may be a result of differing immune status.

Highlights

  • Patients suffering from acute lung injury (ALI) or acute aspiratory distress syndrome (ARDS) are likely to receive mechanical ventilation (MV) treatment as a therapeutic intervention [1]

  • The oxygen index (OI) differed over time in all groups with the lowest PaO2/FiO2 occurring in group CLP1day + LMV, while the highest OI occurred in group CLP4day + MMV

  • MV can amplify the inflammatory response of preinjured lungs or induce massive release of cytokines from healthy lungs [21, 22], a finding that was validated in our current study

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Summary

Introduction

Patients suffering from acute lung injury (ALI) or acute aspiratory distress syndrome (ARDS) are likely to receive mechanical ventilation (MV) treatment as a therapeutic intervention [1]. Sepsis is a critical state of inflammation with high morbidity and mortality rates in the intensive care unit (ICU) [5]. Certain factors, such as overgeneration of reactive oxygen species (ROS), play important roles between sepsis and VILI. Both in vivo and in vitro studies have demonstrated that oxidative stress, plus dysfunction of antioxidant system, leads to the onset or deterioration of ALI after sepsis and VILI [6, 7]. Previous studies have shown that MV had a negative impact on preinjured lungs or other organs affected by sepsis [12,13,14]

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