TY - JOUR
T1 - Ventilator-induced coagulopathy in experimental Streptococcus pneumoniae pneumonia
AU - Haitsma, J. J.
AU - Schultz, M. J.
AU - Hofstra, J. J.H.
AU - Kuiper, J. W.
AU - Juco, J.
AU - Vaschetto, R.
AU - Levi, M.
AU - Zhang, H.
AU - Slutsky, A. S.
PY - 2008/12
Y1 - 2008/12
N2 - 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-expiratory pressure (PEEP)) or MV causing VILI (high tidal volumes (HV T) and zero end-expiratory pressure (ZEEP)) for 3 h. Nonventilated pneumonia rats and healthy rats served as controls. Thrombin-antithrombin complexes (TATc), as a measure for coagulation, and plasminogen activator activity, as a measure of fibrinolysis, were determined in bronchoalveolar lavage fluid (BALF) and serum. Pneumonia was characterised by local (BALF) activation of coagulation, resulting in elevated TATc levels and attenuation of fibrinolysis compared with healthy controls. LVT-PEEP did not influence alveolar coagulation or fibrinolysis. HVT-ZEEP did intensify the local procoagulant response: TATc levels rose significantly and levels of the main inhibitor of fibrinolysis, plasminogen activator inhibitor-1, increased significantly. HVT-ZEEP also resulted in systemic elevation of TATc compared with LVT-PEEP. Mechanical ventilation causing ventilator-induced lung injury increases pulmonary coagulopathy in an animal model of Streptococcus pneumoniae pneumonia and results in systemic coagulopathy. Copyright
AB - 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-expiratory pressure (PEEP)) or MV causing VILI (high tidal volumes (HV T) and zero end-expiratory pressure (ZEEP)) for 3 h. Nonventilated pneumonia rats and healthy rats served as controls. Thrombin-antithrombin complexes (TATc), as a measure for coagulation, and plasminogen activator activity, as a measure of fibrinolysis, were determined in bronchoalveolar lavage fluid (BALF) and serum. Pneumonia was characterised by local (BALF) activation of coagulation, resulting in elevated TATc levels and attenuation of fibrinolysis compared with healthy controls. LVT-PEEP did not influence alveolar coagulation or fibrinolysis. HVT-ZEEP did intensify the local procoagulant response: TATc levels rose significantly and levels of the main inhibitor of fibrinolysis, plasminogen activator inhibitor-1, increased significantly. HVT-ZEEP also resulted in systemic elevation of TATc compared with LVT-PEEP. Mechanical ventilation causing ventilator-induced lung injury increases pulmonary coagulopathy in an animal model of Streptococcus pneumoniae pneumonia and results in systemic coagulopathy. Copyright
KW - Acute respiratory distress syndrome
KW - Biotrauma
KW - Coagulation
KW - Mechanical ventilation
KW - Pneumonia
UR - http://www.scopus.com/inward/record.url?scp=58849097561&partnerID=8YFLogxK
U2 - https://doi.org/10.1183/09031936.00045908
DO - https://doi.org/10.1183/09031936.00045908
M3 - Article
C2 - 18768578
SN - 0903-1936
VL - 32
SP - 1599
EP - 1606
JO - European respiratory journal
JF - European respiratory journal
IS - 6
ER -