Abstract
BackgroundTo examine whether acute lung injury from direct and indirect origins differ in susceptibility to ventilator-induced lung injury (VILI) and resultant systemic inflammatory responses.MethodsRats were challenged by acid instillation or 24 h of sepsis induced by cecal ligation and puncture, followed by mechanical ventilation (MV) with either a low tidal volume (Vt) of 6 mL/kg and 5 cm H2O positive end-expiratory pressure (PEEP; LVt acid, LVt sepsis) or with a high Vt of 15 mL/kg and no PEEP (HVt acid, HVt sepsis). Rats sacrificed immediately after acid instillation and non-ventilated septic animals served as controls. Hemodynamic and respiratory variables were monitored. After 4 h, lung wet to dry (W/D) weight ratios, histological lung injury and plasma mediator concentrations were measured.ResultsOxygenation and lung compliance decreased after acid instillation as compared to sepsis. Additionally, W/D weight ratios and histological lung injury scores increased after acid instillation as compared to sepsis. MV increased W/D weight ratio and lung injury score, however this effect was mainly attributable to HVt ventilation after acid instillation. Similarly, effects of HVt on oxygenation were only observed after acid instillation. HVt during sepsis did not further affect oxygenation, compliance, W/D weight ratio or lung injury score. Plasma interleukin-6 and tumour necrosis factor-α concentrations were increased after acid instillation as compared to sepsis, but plasma intercellular adhesion molecule-1 concentration increased during sepsis only. In contrast to lung injury parameters, no additional effects of HVt MV after acid instillation on plasma mediator concentrations were observed.ConclusionsDuring MV more severe lung injury develops after acid instillation as compared to sepsis. HVt causes VILI after acid instillation, but not during sepsis. However, this differential effect was not observed in the systemic release of mediators.
Highlights
To examine whether acute lung injury from direct and indirect origins differ in susceptibility to ventilator-induced lung injury (VILI) and resultant systemic inflammatory responses
In a clinical study, involving patients suffering from pneumonia, peritonitis or polytrauma, these types of injury differed in terms of respiratory mechanics and response to positive end-expiratory pressure [2]
mechanical ventilation (MV) strategy did not influence Mean arterial pressure (MAP) at baseline, but, as analyzed by the interaction between model and MV, the LVt sepsis group had a lower MAP compared to the HVt acid group at baseline
Summary
To examine whether acute lung injury from direct and indirect origins differ in susceptibility to ventilator-induced lung injury (VILI) and resultant systemic inflammatory responses. Predominant consolidation of the lung in direct injury as opposed to oedema and alveolar collapse in indirect injury might imply the potential for greater ventilator-lung induced injury (VILI) in the former since alveolar recruitability would be less and overdistension greater for a given tidal volume [2,10,11]. One of the consequences of VILI is an increase in translocation of mediators involved in lung inflammation into the systemic circulation, thereby potentially contributing to remote organ injury and failure [15,16,17,18,19,20] It is unknown, whether direct vs indirect injuries differ in this respect, but greater propensity for VILI in the former could be associated with a greater systemic inflammatory response Whether direct vs. indirect injuries differ in this respect, but greater propensity for VILI in the former could be associated with a greater systemic inflammatory response
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