Background: To examine whether acute lung injury from direct and indirect origins differ in susceptibility to\r\nventilator-induced lung injury (VILI) and resultant systemic inflammatory responses.\r\nMethods: Rats were challenged by acid instillation or 24 h of sepsis induced by cecal ligation and puncture,\r\nfollowed by mechanical ventilation (MV) with either a low tidal volume (Vt) of 6 mL/kg and 5 cm H2O positive\r\nend-expiratory pressure (PEEP; LVt acid, LVt sepsis) or with a high Vt of 15 mL/kg and no PEEP (HVt acid, HVt\r\nsepsis). Rats sacrificed immediately after acid instillation and non-ventilated septic animals served as controls.\r\nHemodynamic and respiratory variables were monitored. After 4 h, lung wet to dry (W/D) weight ratios, histological\r\nlung injury and plasma mediator concentrations were measured.\r\nResults: Oxygenation and lung compliance decreased after acid instillation as compared to sepsis. Additionally, W/\r\nD weight ratios and histological lung injury scores increased after acid instillation as compared to sepsis. MV\r\nincreased W/D weight ratio and lung injury score, however this effect was mainly attributable to HVt ventilation\r\nafter acid instillation. Similarly, effects of HVt on oxygenation were only observed after acid instillation. HVt during\r\nsepsis did not further affect oxygenation, compliance, W/D weight ratio or lung injury score. Plasma interleukin-6\r\nand tumour necrosis factor-a concentrations were increased after acid instillation as compared to sepsis, but\r\nplasma intercellular adhesion molecule-1 concentration increased during sepsis only. In contrast to lung injury\r\nparameters, no additional effects of HVt MV after acid instillation on plasma mediator concentrations were\r\nobserved.\r\nConclusions: During MV more severe lung injury develops after acid instillation as compared to sepsis. HVt causes\r\nVILI after acid instillation, but not during sepsis. However, this differential effect was not observed in the systemic\r\nrelease of mediators.
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