Blood Platelet Activation and Membrane Glycoprotein Changes during Extracorporeal Life Support (Ecls). In Vitro Studies

Abstract

The aim of this study was to evaluate an in vitro model for investigation of platelet function parameters in an extracorporeal system. Two different perfusion pumps were compared, a roller pump (Polystan) and a centrifugal pump (Biomedicus). A continuous increase in glycoprotein (GP)1b-negative platelets was observed in both circuits. A marked increase of plasma beta-thromboglobulin thromboglobulin concentration and a decrease of the intracellular pool of serotonin was observed, indicating a marked release of alpha as well as of dense granules. The plasma concentration of glycocalicin increased in parallel with a reduced platelet surface expression of GP1b, suggesting that the loss of GP1b is caused by proteolysis rather than by a downregulation of this receptor protein. It is concluded that ECLS results in a pronounced platelet degranulation and causes changes of important membrane receptors which might explain some of the bleeding problems observed in patients treated with ECLS. No significant difference was noted between the roller pump and the centrifugal pump. Trial of strategies, e.g., protease inhibitors and nitric oxide to revert this untoward effect of ECLS are highly warranted.

The attenuation of platelet and monocyte activation in a rabbit model of extracorporeal circulation by a nitric oxide releasing polymer

“…By utilizing NO as the agent being released from the diazeniumdiolated polymer in this study, the degree of thrombosis and ECC-induced expression of platelet P-selectin and monocyte CD11b were attenuated. Much of ECLS research has previously shown a decrease in the levels of thrombosis and an underlying threshold level of locally-released NO from either polyvinyl chloride (PVC) or polyurethane (PU)-based polymers [25,26,56–58]. Skrzypchak et al, in particular, had shown that the NO donor, DBHD/N 2 O 2 released an amount of NO from the PVC polymer that preserved platelet number and maintained their ability to aggregate upon stimulation with exogenous collagen [26].…”

Platelet activation and degradation in an experimental extracorporeal system. A comparison between a silicone membrane and a hollow-fibre oxygenator

“…3,4 Indeed, already during the first minutes of perfusion, contact between blood and biomaterial induces an activation of various cascade systems. 3,5,6 Over the past few years, much effort has been devoted to improving the biocompatibility of extracorporeal systems, e.g. the use of heparinized perfusion circuits?…”

The effect of albumin priming solution on platelet activation during experimental long-term perfusion

“…Most likely, these re-appearing platelets have lost much of their a-granula content, and circulate as nonfunctional platelet ghosts. 1 We conclude that albumin priming appears to prevent platelet activation during long-term extracorporeal circulation. Furthermore, albumin coating might even reduce the initial adherence of platelets to the foreign material of the circuit.…”

“…The bleeding complications seen in association with ECMO treatment have been attributed to the systemic heparinization, as well as to an induced thrombocytopenia and platelet dysfunction. 1 Albumin coating is routinely used to passivate the surfaces of extracorporeal perfusion systems and it has been assumed that this treatment preserves the platelets and inhibits platelet adhesion to the artificial surfaces. However, this effect of albumin priming has, to our knowledge, not been demonstrated under controlled conditions.…”