Activated neutrophils and platelet microaggregates impede blood filterability through microchannels during simulated extracorporeal circulation

2003 ◽  
Vol 75 (4) ◽  
pp. 1254-1260 ◽  
Author(s):  
Yukihiro Yoshimura ◽  
Yuji Hiramatsu ◽  
Yukio Sato ◽  
Satoshi Homma ◽  
Yoshiharu Enomoto ◽  
...  
Keyword(s):  
Extracorporeal Circulation ◽  
Activated Neutrophils ◽  
Blood Filterability

Experimental study of total body washout employing extracorporeal circulation and hypothermia

1974 ◽  
Vol 126 (2) ◽  
pp. 243-248
Author(s):  
A WAKABAYASHI ◽  
T KUBO ◽  
K CHARNEY ◽  
Y NAKAMURA ◽  
J CONNOLLY
Keyword(s):  
Experimental Study ◽  
Extracorporeal Circulation ◽  
Total Body

Influence of lipid and leucocyte separation on patient inflammatory response during extracorporeal circulation

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
TE Siegle ◽  
I Friedrich ◽  
A Paraforos ◽  
G Haimerl ◽  
W Olmscheid ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Extracorporeal Circulation

The Hemostatic Mechanism after Open-Heart Surgery

1978 ◽  
Vol 39 (02) ◽  
pp. 474-487 ◽  
Author(s):  
E R Cole ◽  
F Bachmann ◽  
C A Curry ◽  
D Roby
Keyword(s):  
Extracorporeal Circulation ◽  
Heart Surgery ◽  
Polyacrylamide Gel Electrophoresis ◽  
Open Heart Surgery ◽  
Coagulation System ◽  
Open Heart ◽  
Time Activity ◽  
Post Surgery ◽  
Plasma Fractions ◽  
The Mean

SummaryA prospective study in 13 patients undergoing open-heart surgery with extracorporeal circulation revealed a marked decrease of the mean one-stage prothrombin time activity from 88% to 54% (p <0.005) but lesser decreases of factors I, II, V, VII and X. This apparent discrepancy was due to the appearance of an inhibitor of the extrinsic coagulation system, termed PEC (Protein after Extracorporeal Circulation). The mean plasma PEC level rose from 0.05 U/ml pre-surgery to 0.65 U/ml post-surgery (p <0.0005), and was accompanied by the appearance of additional proteins as evidenced by disc polyacrylamide gel electrophoresis of plasma fractions (p <0.0005). The observed increases of PEC, appearance of abnormal protein bands and concomitant increases of LDH and SGOT suggest that the release of an inhibitor of the coagulation system (similar or identical to PIVKA) may be due to hypoxic liver damage during extracorporeal circulation.

Neutrophil Derived Cathepsin G Induces Potentially Thrombogenic Changes in Human Endothelial Cells: a Scanning Electron Microscopy Study in Static and Dynamic Conditions

1994 ◽  
Vol 72 (01) ◽  
pp. 140-145 ◽  
Author(s):  
Valeri Kolpakov ◽  
Maria Cristina D'Adamo ◽  
Lorena Salvatore ◽  
Concetta Amore ◽  
Alexander Mironov ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Thrombus Formation ◽  
Cathepsin G ◽  
Arterial Segment ◽  
Dynamic Conditions ◽  
Activated Neutrophils ◽  
Scanning Electron

SummaryActivated neutrophils may promote thrombus formation by releasing proteases which may activate platelets, impair the fibrinolytic balance and injure the endothelial monolayer.We have investigated the morphological correlates of damage induced by activated neutrophils on the vascular wall, in particular the vascular injury induced by released cathepsin G in both static and dynamic conditions.Human umbilical vein endothelial cells were studied both in a cell culture system and in a model of perfused umbilical veins. At scanning electron microscopy, progressive alterations of the cell monolayer resulted in cell contraction, disruption of the intercellular contacts, formation of gaps and cell detachment.Contraction was associated with shape change of the endothelial cells, that appeared star-like, while the underlying extracellular matrix, a potentially thrombogenic surface, was exposed. Comparable cellular response was observed in an “in vivo” model of perfused rat arterial segment. Interestingly, cathepsin G was active at lower concentrations in perfused vessels than in culture systems. Restoration of blood flow in the arterial segment previously damaged by cathepsin G caused adhesion and spreading of platelets on the surface of the exposed extracellular matrix. The subsequent deposition of a fibrin network among adherent platelets, could be at least partially ascribed to the inhibition by cathepsin G of the vascular fibrinolytic potential.This study supports the suggestion that the release of cathepsin G by activated neutrophils, f.i. during inflammation, may contribute to thrombus formation by inducing extensive vascular damage.

Sign in / Sign up

Export Citation Format

Share Document