Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury

@article{Dahlem2006MechanicalVA,
  title={Mechanical ventilation affects alveolar fibrinolysis in LPS-induced lung injury},
  author={Peter Dahlem and Albert P. Bos and Jack J. Haitsma and Marcus J. Schultz and E. K. Wolthuis and Joost C. M. Meijers and Burkhard Lachmann},
  journal={European Respiratory Journal},
  year={2006},
  volume={28},
  pages={992 - 998}
}
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… 
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References

SHOWING 1-10 OF 35 REFERENCES
Alveolar fibrinolytic capacity suppressed by injurious mechanical ventilation
TLDR
Alveolar fibrinolytic capacity is suppressed during mechanical ventilation with high pressure amplitudes due to local production of PAI-1.
Ventilator-induced heat shock protein 70 and cytokine mRNA expression in a model of lipopolysaccharide-induced lung inflammation
TLDR
It is proposed that HSP70 expression protects the lung against ventilator-induced lung injury by decreasing cytokine transcription in the lung.
Alveolar fibrin formation caused by enhanced procoagulant and depressed fibrinolytic capacities in severe pneumonia. Comparison with the acute respiratory distress syndrome.
TLDR
Acute inflammatory lung injury, whether triggered by nonpulmonary systemic events or primary lung infection, is thus consistently characterized by both enhanced procoagulant and depressed fibrinolytic activities in the alveolar lining layer, with the appearance of fibrin formation in this compartment.
Priming for enhanced alveolar fibrin deposition after hemorrhagic shock: role of tumor necrosis factor.
TLDR
A cellular and molecular basis for lung fibrin deposition after resuscitated shock is provided and a divergence of pathways responsible for fibr in generation and neutrophil accumulation is demonstrated.
Exogenous Surfactant Preserves Lung Function and Reduces Alveolar Evans Blue Dye Influx in a Rat Model of Ventilation‐induced Lung Injury
TLDR
Data indicate that surfactant has a beneficial effect on ventilation‐induced lung injury and prevents impairment of oxygenation, lung mechanics, and minimal surface tension of bronchoalveolar lavage fluid and reduces alveolar influx of Evans blue dye.
Plasminogen activator inhibitor-1 in acute hyperoxic mouse lung injury.
TLDR
It is shown that lungs of mice exposed to hyperoxia overproduce plasminogen activator inhibitor-1 (PAI-1), and that PAI- 1 upregulation impairs fibrinolytic activity in the alveolar compartment, and these observations provide clear and novel evidence for the pathogenic contribution of PAi-1 in the development of hyaline membrane disease.
Pulmonary coagulopathy as a new target in therapeutic studies of acute lung injury or pneumonia—A review
TLDR
Theoretical considerations suggest that this anticoagulant therapy will benefit patients with primary lung pathology including VILI, but clinical studies are needed to examine this hypothesis before such therapy is to be advocated as a standard of care in critically ill patients.
Intratracheal aerosolization of endotoxin (LPS) in the rat: a comprehensive animal model to study adult (acute) respiratory distress syndrome.
TLDR
It is suggested that intratracheal LPS administration mimics the clinical development of ARDS very closely.
Coagulation and inflammation in acute lung injury.
TLDR
New interventional strategies directed at procoagulant activity highlight the importance of the coagulation system to acute lung injury and suggest that blockade of initiation of coagulations may have therapeutic benefit in patients with ARDS.
Elevated levels of plasminogen activator inhibitor-1 in pulmonary edema fluid are associated with mortality in acute lung injury.
TLDR
PAI-1 levels in edema fluid and plasma identify those with ALI that have a poor prognosis, and fibrin turnover in early ALI is a consequence of a rapidfibrinogen influx and fractional fibrinolytic inhibition.
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