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• W1996207798 abstract "In vivo 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 cmH2O], 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." @default.
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• W1996207798 date "2003-11-01" @default.
• W1996207798 modified "2023-10-14" @default.
• W1996207798 title "Injurious ventilation strategies cause systemic release of IL-6 and MIP-2 in rats <i>in vivo</i> *" @default.
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• W1996207798 doi "https://doi.org/10.1046/j.1475-0961.2003.00518.x" @default.
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