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In this laboratory study, acute respiratory distress syndrome was induced by acid aspiration in 24 rabbits which were then randomised to injurious (tidal volume 15–17 ml/kg, PEEP 0–3 cm H2O) or non-injurious ventilation (tidal volume 5–7 ml/kg, PEEP 9–12 cm H2O). Serum levels of chemokines putatively associated with ventilator induced lung injury and involved in renal apoptosis (monocyte chemotactic protein 1, IL-8 and growth regulated oncogene) together with LDH, AST and creatinine were all significantly higher in the injurious strategy group. The apoptotic index was increased in renal tubules and small intestinal villi from 1.86% and 0.97% (non-injurious) to 10.9% and 6.7% (injurious). Plasma from the rabbits ventilated by the injurious strategy induced more apoptosis in a culture of renal proximal tubule cells. The degree of apoptosis was reduced by binding soluble Fas ligand. Using plasma from human subjects in an earlier study of protective ventilation, soluble Fas ligand was higher in those ventilated by an injurious strategy and changes in its level correlated with changes in creatinine over 72 hours.
This study shows that injurious mechanical ventilation can induce apoptosis in distal organs and may contribute to the development of multiple organ dysfunction. It suggests mediation by circulating pro-apoptotic factors such as soluble Fas ligand.
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