scholarly journals Bronchoalveolar Activation of Coagulation and Inhibition of Fibrinolysis during Ventilator-Associated Lung Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-8
Author(s):  
M. J. Schultz ◽  
R. M. Determann ◽  
A. A. N. M. Royakkers ◽  
E. K. Wolthuis ◽  
J. C. Korevaar ◽  
...  

Background and Objective. Bronchoalveolar coagulopathy is a characteristic feature of pulmonary inflammation. We compared bronchoalveolar and systemic levels of coagulation in patients who did and patients who did not develop ventilator-associated lung injury (VALI).Methods. Secondary analysis of a randomized controlled trial evaluating the effect of lower tidal volumes versus conventional tidal volumes in patients without acute lung injury or acute respiratory distress syndrome at the onset of mechanical ventilation.Results. Ten patients with VALI and 10 random control patients without lung injury during the course of mechanical ventilation, but all ventilated with conventional tidal volumes, were compared. Patients who developed VALI showed both bronchoalveolar activation of coagulation (increase in thrombin–antithrombin complex levelsP<0.001versus baseline) and inhibition of fibrinolysis (decline in plasminogen activator activityP<0.001versus baseline). The later seemed to be dependent on higher levels of plasminogen activator inhibitor type 1 (P=0.001versus baseline). Patients who developed VALI also showed elevated systemic thrombin-antithrombin complex levels and decreased systemic plasminogen activator activity levels.Conclusions. VALI is characterized by bronchoalveolar coagulopathy. Systemic and bronchoalveolar coagulopathy at the onset of mechanical ventilation may be a risk factor for developing VALI in patients ventilated with conventional tidal volumes.

1970 ◽  
Vol 19 (2) ◽  
pp. 87-93
Author(s):  
MS Kabir ◽  
AAS Majumder ◽  
AW Chowdhury ◽  
SA Haque ◽  
AQM Reza ◽  
...  

Only one half to two thirds of atherosclerotic vascular diseases can be explained by classical risk factors like smoking, diabetes mellitus, hypertension, dyslipidaemia, family history of premature atherosclerotic vascular diseases, physical inactivity, obesity etc. Some other variables appear to contribute to the development of atherosclerotic vascular diseases which include estrogen deficiency, lipoprotein (a), plasma fibrinogen, plasminogen-activator inhibitor type I, endogenous tissue plasminogen activator (tPA), C-reactive protein and homocysteine. Over the last several years, investigators undertook extensive research work, in home and abroad, to determine the contribution of plasma homocysteine in the pathogenesis of atherosclerotic vascular diseases. So far the research work indicates, raised plasma homocysteine appears to be a potential risk factor for ischaemic heart disease.   doi: 10.3329/taj.v19i2.3158 TAJ 2006; 19(2): 87-93


Sign in / Sign up

Export Citation Format

Share Document