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Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury

¹ Dept of Anaesthesiology, Erasmus MC-Faculty Rotterdam, Rotterdam, and ² Emma Children's Hospital, Paediatric Intensive Care Unit, ⁴ Adult Intensive Care Unit, and ⁵ Dept of Vascular Medicine, Academic Medical Centre of the University of Amsterdam, Amsterdam, The Netherlands. ³ Interdepartmental Division of Critical Care, University of Toronto, Toronto, ON, Canada.

CORRESPONDENCE: P. Dahlem, Coburg Medical Centre, Children's Hospital, Ketschendorferstr. 33, 96450 Coburg, Germany. Fax: 49 9561225552. E-mail: PDahlem{at}hotmail.com

Keywords: Adult respiratory distress syndrome, animal experimentation, endotoxin, fibrinolysis, mechanical ventilation

Received: November 21, 2004
Accepted June 30, 2006

The aim of the present study was to determine the effects of mechanical ventilation on alveolar fibrin turnover in lipopolysaccharide (LPS)-induced lung injury.

In a randomised controlled trial, Sprague–Dawley rats (n = 61) were allocated to three ventilation groups after intratracheal LPS (Salmonella enteritidis) instillations. Group I animals were subjected to 16 cmH₂O positive inspiratory pressure (PIP) and 5 cmH₂O positive end-expiratory pressure (PEEP); group II animals to 26 cmH₂O PIP and 5 cmH₂O PEEP; and group III animals to 35 cmH₂O PIP and 5 cmH₂O PEEP. Control rats (not mechanically ventilated) received LPS. Healthy rats served as a reference group. Levels of thrombin–antithrombin complex (TATc), D-dimer, plasminogen activator inhibitor (PAI) activity and PAI-1 antigen in bronchoalveolar lavage fluid were measured.

LPS-induced lung injury increased TATc, D-dimer and PAI activity and PAI-1 antigen levels versus healthy animals. High pressure-amplitude ventilation increased TATc concentrations. D-dimer concentrations were not significantly raised. Instead, PAI activity increased with the amplitude of the pressure, from 0.7 U·mL^-1 in group I to 3.4 U·mL^-1 in group II and 5.0 U·mL^-1 in group III. There was no change in PAI-1 antigen levels.

In conclusion, mechanical ventilation creates an alveolar/pulmonary anti-fibrinolytic milieu in endotoxin-induced lung injury which, at least in part, might be due to an increase in plasminogen activator inhibitor activity.

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