Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury

¹ Dept of Anaesthesiology, Erasmus MC-Faculty Rotterdam; and Emma Children's Hospital, paediatric Intensive Care Unit
² Emma Children's Hospital, paediatric Intensive Care Unit
³ Dept of Anaesthesiology, Erasmus MC-Faculty Rotterdam
⁴ Adult Intensive Care Unit
⁵ Dept of Vascular Medicine, Academic Medical Centre of the University of Amsterdam, The Netherlands

^* To whom correspondence should be addressed. E-mail: PDahlem{at}hotmail.com.

	Abstract

The effects of mechanical ventilation on alveolar fibrinolysis in lipopolysaccharide (LPS)-induced lung injury.

Randomized controlled trial. After intratracheal LPS (Salmonella enteritidis) instillations Sprague-Dawley rats (n=61) were allocated to 3 ventilation groups. Group I: positive inspiratory pressure (PIP) 16 cm H2O/positive end-expiratory pressure (PEEP) 5 cm H2O; group II: PIP 26 cm H2O/PEEP 5 cm H2O and group III: PIP 35 cm H2O/PEEP 5 cm H2O. Control rats (not mechanically ventilated) received LPS. Healthy rats served as reference group.

Thrombin anti-thrombin complexes (TATc), D-dimer and plasminogen activator inhibitor (PAI)-1in broncho-alveolar lavage fluid (BALF). Results were adjusted for total protein content in BALF.

TATc increased from 3.35 ng·mL^-1 (95% confidence interval 0.92-5.83) in healthy animals to 76.28 ng·mL^-1 (4.65-107.12) in LPS controls (p<0.001); D-dimer levels were 1.75 µg·mL^-1 (0.73-3.27) vs. 13.36 µg·mL^-1 (8.82-17.90) respectively. Adjusted D-dimer were in group I 40.02 µg·L^-1 (21.98-58.06), in group II 37.32 µg·L^-1 (20.23-54.40) and in group III 50.83 µg·L^-1 (30.72-70.94) (p=0.041, NS). In contrast, adjusted PAI-1 activity increased in group I 1.00 U·mL^-1 (0.03-1.97), group II 3.19 U·mL^-1 (2.38-4.01) and in group III 3.54 U·mL^-1 (2.43-4.65) (p<0.000).

Mechanical ventilation increased alveolar PAI-1 activity which might suppress alveolar fibrinolysis.

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