Beschreibung:
<jats:title>Summary</jats:title><jats:p> <jats:italic>In vivo</jats:italic> experiments showed no increased production of tumour necrosis factor (TNF) in response to injurious ventilation strategies in otherwise untreated animals. Because interleukin‐6 (IL‐6) and macrophage inflammatory protein‐2 (MIP‐2) are more sensitive markers of ventilation‐induced cytokine release, serum and bronchoalveolar lavage (BAL) samples were examined for these mediators. Eighty‐five adult rats were randomized to three different ventilation strategies. Rats were ventilated with low pressures and low tidal volumes [13/3; peak inspiratory pressure (PIP)/positive end‐expiratory pressure (PEEP) in cmH<jats:sub>2</jats:sub>O], the second group of rats was ventilated with high pressures and low PEEP resulting in high tidal volumes (32/6), and the third group was ventilated with the same high pressures but without PEEP (32/0). Animals were ventilated either for 90 or 240 min, subsequently serum and BAL were collected for analyses on IL‐6 and MIP‐2 content. Non‐ventilated animals served as healthy controls. Ventilation with 32/0 for 90 or 240 min, led to increased serum IL‐6 levels. Serum MIP‐2 levels were increased by ventilation with 32/6 (90 min) and 32/0 (240 min). Ventilation under any condition, even at 13/3, resulted in elevated MIP‐2 levels in the BAL fluid. Even at normal pressures pulmonary MIP‐2 levels were increased, suggesting that ventilation may promote pro‐inflammatory responses in healthy subjects.</jats:p>