Sarah Blair
Research Scientist
SUNY Upstate Medical University
Syracuse, NY
Disclosure information not submitted.
Joshua Satalin, BA
Research Scientist
SUNY Upstate Medical University
Syracuse, New York, United States
Disclosure information not submitted.
Penny Andrews, RN
Registered Nurse
University of Maryland, United States
Disclosure information not submitted.
Nader Habashi, MD
Professor
R. Adams Cowley Shock Trauma Center
Baltimore, United States
Disclosure information not submitted.
Louis Gatto, PhD
Professor
SUNY Upstate Medical University, United States
Disclosure information not submitted.
Jason Bates, PhD
Professor
University of Vermont, United States
Disclosure information not submitted.
Gary Nieman, BA
Professor
SUNY Upstate Medical University, United States
Disclosure information not submitted.
Michaela Kollisch-Singule, MD
Assistant Professor
SUNY Upstate Medical University, United States
Disclosure information not submitted.
Title: Excessive Dynamic and Static Strain Act Synergistically To Increase Lung Inflammation
Introduction: Severe systemic inflammation is a major mechanism of acute respiratory distress syndrome (ARDS). Patients with ARDS may need mechanical ventilation (MV) to support the lungs, however improperly set MV can exacerbate inflammation causing a biotrauma-mediated ventilator induced lung injury (VILI). Understanding the pro-inflammatory effects of different MV strategies is critical to reducing VILI and may serve as early biomarkers of lung injury.
Methods: Yorkshire pigs were anesthetized, instrumented, and lung injury was induced by bronchoscopic instillation of 3% Tween into the dependent lung lobes. The animals were placed on APRV with an inspiratory duration (THigh) of 4.0s and an expiratory pressure (PLow) of 0cmH2O. They were randomized to varying inspiratory pressures (PHigh) and expiratory durations (TLow) set to induce high dynamic strain, high static strain, both, or neither: DS (n=10: P<sub>High 28cmH2O, TLow set to terminate expiratory flow at 25% of peak expiratory flow [TPEF]); SS (n=10: P<sub>High 40cmH2O, 75% TPEF); DS+SS (n=10: P<sub>High 40cmH2O, 25% TPEF); Non-DS/SS (Time Controlled Adaptive Ventilation (TCAV™) Method) (n=10: P<sub>High 28cmH2O, 75% TPEF). Animals were sacrificed after 6 hours and the left dependent lobe was preserved in Qiagen RNAprotect for mRNA analysis by quantitative real time PCR.
Results: The Non-DS/SS and DS groups showed a significant decrease in IL8 expression (p< 0.05) as compared to the DS+SS group. IL1B showed an increase in expression in the SS and DS+SS groups as compared to the Non-DS/SS and DS groups, although not reaching statistical significance (p >0.05).
Conclusions: Although it is well-accepted that MV can lead to VILI, the impact of excessive dynamic and static strain on lung inflammation has not been fully characterized. In this study, the combination of DS and SSled to pro-inflammatory cytokine IL8 and IL1B expression, but DS alone did not. These results suggest that SSmay play a greater role in propagating biotrauma as compared with DS and, further, that IL8 and IL1B elevation may serve as biomarkers indicating SS.
Funded R01HL142702 and W81XWH2010696