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

Abstract

The objective of this study was to evaluate the effect of albumin priming on platelet consumption and activation during long-term perfusion. Two identical in vitro extracorporeal membrane oxygenation circuits were used; one was primed with Ringer's solution containing human serum albumin, the other with Ringer's solution only. Fresh heparinized human blood was pooled, divided between the two systems and circulated for 24 h at 37 degrees C. Platelet count, plasma concentration of betathromboglobulin (BTG), platelet membrane density of glycoprotein (GP) Ib and of GPIIb/IIIa were assayed before the start and at 0.5, 1, 3, 12 and 24 h of perfusion. In total, seven experiments were performed. We found that during the first hour of perfusion, slightly higher platelet counts (p = 0.058) and lower BTG values (p = 0.0005) were observed in the circuits primed with albumin, compared to the control circuits. No statistically significant differences were observed for the platelet membrane expression of GPIb and GPIIb/IIIa. We conclude that albumin priming appears to transiently prevent platelet consumption and activation during long-term perfusion.

Effect of 6% Hydroxyethyl Starch 130/0.4 as a Priming Solution on Coagulation and Inflammation Following Complex Heart Surgery

“…The only adverse influence of human albumin on coagulation seems to stem from its subsequent hemodilutional effect 2,3,4. Furthermore, when used for priming, albumin forms a layer on the surface of the CPB circuit, making it less thrombogenic, which decreases the affinity of the platelets, leading to their preservation 24. In terms of inflammation, albumin has been shown to inhibit apoptosis5 and attenuate the inflammatory response 25.…”

In vitro hemocompatibility of albumin–heparin multilayer coatings on polyethersulfone prepared by the layer‐by‐layer technique

“…Only very few direct comparisons of albuminated and heparinized surfaces exist in the literature. The precoating of blood‐contacting surfaces with albumin, usually achieved by simple priming with albumin solution, is known to improve the platelet response, at least temporarily 19–22. We observed earlier that albumin coatings on Dacron vascular prostheses effectively suppressed platelet depletion from whole blood slightly more effectively than the albumin–heparin coatings 17.…”

“…To achieve this we developed a method for the coating of solid surfaces with a defined number of molecular layers of albumin and heparin 13–18. Albumin, the most abundant blood plasma protein, reduces undesirable nonspecific interactions of the surface with blood plasma proteins 19–22…”

In Vitro Thrombogenicity Testing of Biomaterials

“…The degree of unfolding and associated exposition of platelet binding sites (located at the fibrinogen γ‐chain and α‐chain) correlate with the activation and adhesion of platelets to material surfaces, while they do not with the amount of adsorbed fibrinogen . This seems to represent a fundamental concept since analogous reports are available for proteins, which are not involved in the cascade systems and considered to reduce the thrombogenic potential of device surfaces, such as albumin . Similarly to fibrinogen, albumin mediates the adhesion of platelets to material surfaces via RGD‐specific receptors if the protein exhibited a certain degree of unfolding .…”