Extra Corporel Membrane Oxygenation and Mciroparticles Clinical Trial
ECMO (extra-corporeal membrane oxygenation) is a blood oxygenation technical and
purification of carbon dioxide by means of an extracorporeal circulation using a pump
(identical to those used in cardiac surgery) and a membrane permitting gas exchange. This
technique is used for almost 40 years in the acute respiratory distress syndrome (ARDS) but
benefited from many technology improvements over the past 10 years.
The circuit is now fully pre-heparin, not imposing obtaining activated partial
thromboplastin time (aPTT) high. Centrifugal pumps limit the risk of intravascular
hemolysis. The multi-perforated drainage cannula in place in femoral vein or jugular no
longer need to maintain hypervolaemia to ensure sufficient flow.
The membrane ensuring gas exchange is now polymethylpentene. This hollow fiber system
ensures the gas exchange.
In light of recent technical improvements, manufacturers indicate that the membranes can be
used for 3 weeks. However, after a few days of use, fibrinoplaquettaires microthrombi form
at the ECMO circuit, up from cannulas up to the oxygenator, decreasing membrane efficiency
and imposing more early changes of the circuit. This hypercoagulable state was revealed
through the study of classical plasma markers of coagulation. There is not so far from
reliable predictive marker of thrombus formation, indicating a need to change the circuit.
The production of microparticles (MPs) is a characteristic of cells subjected to an
activation or apoptosis. MPs are membrane Smaller fragments released into the extracellular
milieu after rupture of the asymmetry of the distribution of membrane phospholipids and
characterized by the presence of phosphatidylserine (PhtdSer) on their surface, as well as
various antigens expressed by their cells of origin. The PhtdSer is a pro-coagulating
surface on which are going to assemble the enzymes responsible for the formation of thrombin
and increases proportionally the TF activity ultimately leading to fibrin polymerization in
the vessels.
The vesiculation phenomenon exists in healthy subjects. In human pathology, many examples
emphasize the fundamental role of MP in clotting or thrombosis. The PM generating fault is
associated with bleeding disorders (Scott syndrome, dysvésiculation syndrome). Conversely,
high circulating levels of MP are found in many thrombotic diseases (myocardial infarction,
diabetes, antiphospholipid antibody syndrome, preeclampsia ...). Platelet and intense
monocyte endothelial activation, observed in sepsis and severe trauma, is accompanied by the
generation of procoagulant MP carriers of tissue factor (TF). These MP diffuse into the
vascular compartment pathogenic potential may exacerbate inflammatory and thrombotic
responses and play a leading role in triggering the DIC.
More recently, various studies have shown that the microparticles are not only activation
markers or injury, but also cellular elements having a true pathogenic role. Because they
contain or express on their surface various biological effector (adhesion molecules, tissue
factor, inflammatory mediators or apoptogenic, growth factor ...) the microparticles are
able to interact with their environment and modulate cellular very different way the
properties of target cells. And platelet or leukocyte microparticles could actively
participate in the thrombotic process by increasing adhesion of monocytes and endothelial
cells, or by inducing endothelial procoagulant response.
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