2008
DOI: 10.1183/09031936.00045908
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Ventilator-induced coagulopathy in experimental Streptococcus pneumoniae pneumonia

Abstract: Pneumonia, the main cause of acute lung injury, is characterised by a local proinflammatory response and coagulopathy. Mechanical ventilation (MV) is often required. However, MV can lead to additional injury: so-called ventilator-induced lung injury (VILI). Therefore, the current authors investigated the effect of VILI on alveolar fibrin turnover in Streptococcus pneumoniae pneumonia.Pneumonia was induced in rats, followed 48 h later by either lung-protective MV (lower tidal volumes (LVT) and positive end-expi… Show more

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Cited by 22 publications
(30 citation statements)
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References 34 publications
(47 reference statements)
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“…Moreover, MV with higher tidal volume and PEEP was associated with higher levels of soluble TM, TF, TAT, fVIIa, and lower levels of APC in BALF, reflecting a procoagulant activity [43] . Haitsma et al [44] have shown, in an animal model of Streptococcus pneumonia, that the implementation of high tidal volume MV was associated with local activation of coagulation and attenuation of fibrinolysis in the lung, whereas the levels of IL-6 in BALF were increased. The abovementioned phenomenon was described as "ventilator-induced coagulopathy."…”
Section: Immunothrombosis In Ards Pathophysiologymentioning
confidence: 99%
“…Moreover, MV with higher tidal volume and PEEP was associated with higher levels of soluble TM, TF, TAT, fVIIa, and lower levels of APC in BALF, reflecting a procoagulant activity [43] . Haitsma et al [44] have shown, in an animal model of Streptococcus pneumonia, that the implementation of high tidal volume MV was associated with local activation of coagulation and attenuation of fibrinolysis in the lung, whereas the levels of IL-6 in BALF were increased. The abovementioned phenomenon was described as "ventilator-induced coagulopathy."…”
Section: Immunothrombosis In Ards Pathophysiologymentioning
confidence: 99%
“…11 Haitsma and colleagues demonstrated that injurious ventilation settings increased pulmonary coagulopathy in an animal model of Streptococcus pneumoniae pneumonia, which resulted in a systemic coagulopathy. 12 Coagulation dysfunction with both defective inhibition of coagulation and attenuation of fibrinolysis could potentially contribute to the development of VTE in ventilated patients. 11,12 Review articles pressure of oxygen and possibly, release of mediators such as platelet-activating factor.…”
Section: Vte and Mechanical Ventilationmentioning
confidence: 99%
“…12 Coagulation dysfunction with both defective inhibition of coagulation and attenuation of fibrinolysis could potentially contribute to the development of VTE in ventilated patients. 11,12 Review articles pressure of oxygen and possibly, release of mediators such as platelet-activating factor. [15][16][17] In patients without pre-existing cardiopulmonary disease who are ventilated to near normal functional residual capacity without significant changes in lung volume and with positive end-expiratory pressure (PEEP) of less than 10 cm H 2 O, clinically important changes in RV afterload are uncommon.…”
Section: Vte and Mechanical Ventilationmentioning
confidence: 99%
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“…Mechanical and inflammatory processes most likely interact: a mechanically stressed lung may produce an inflammatory reaction. Conversely, inflammation renders the lung susceptible to mechanical stress [12]. …”
Section: Introductionmentioning
confidence: 99%