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Comparison of microscopic methods for evaluating platelet adhesion to biomaterial surfaces

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Okrój W. , Walkowiak-Przybyło M. , Rośniak-Bąk K. , Klimek L. , Walkowiak B.

2009

tom Vol. 11, nr 2

45-49

Microscopic methods usable for sample surface imaging and subsequent qualitative and quantitative evaluation of platelet adhesion to the surface of the biomaterial studied were compared. It was shown, making use of the samples of medical steel (AISI 316L), that such tools as surface imaging with scanning electron microscopy (SEM), glutaraldehyde induced fluorescence technique (GIFT) and metallurgical microscopy (MM) are equivalent in evaluating surface platelet adhesion. The importance of biological variability of blood samples for a proper result assessment and the necessity of using internal standards were also considered.

The involvement of Naplus-Kplus-ATPase in the development of platelet procoagulant response

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Tomasiak M. , Stelmach H. , Rusak T. , Ciborowski M. , Radziwon P.

tom 54

nr 3

In circulation, platelets may come into contact with both exogenous (cardiac glycoside treatment) and endogenously produced inhibitors of Na+/K+-ATPase. We examined whether blocking of platelet Na+/K+-ATPase by ouabain results in generation of procoagulant activity. It was shown that an in vitro treatment of platelets with ouabain (20-200 µM for 20 to 60 min) is associated with an intracellular accumulation of sodium ([Na+]i), generation of a weak calcium signal, and expression of procoagulant activity. The ouabain-induced procoagulant response was dose- and time-related, less pronounced than that evoked by collagen and similar to that produced by gramicidin, not affected by EDTA or aspirin, and strongly reduced in the absence of extracellular Na+ or by hyperosmolality. Flow cytometry studies revealed that ouabain treatment results in a unimodal left shift in the forward and side scatter of the entire platelet population indicating morphological changes of the plasma membrane. The shift was dose related, weaker than that evoked by collagen and similar to that produced by gramicidin. Ouabain-treated platelets express phosphatidylserine (PS). The ouabain-evoked PS expression was dose- and time-dependent, weaker than that produced by collagen and similar to that evoked by gramicidin. Electronic cell sizing measurements showed a dose-dependent increase in mean platelet volume upon treatment with ouabain. Hypoosmotically-evoked platelet swelling resulted in the appearance of procoagulant activity. Thromboelastography measurements indicate that, in whole blood, nanomolar (50-1000 nM, 15 min) concentrations of ouabain significantly accelerate the rate of clot formation initiated by contact and high extracellular concentration of calcium. We conclude that inefficiently operating platelet Na+/K+-ATPase results in a rise in [Na+]i. An increase in [Na+]i and the swelling associated with it may produce PS exposure and a rise in membrane curvature leading to the generation of a procoagulant activity.

Sphingosine 1-phosphate is a blood constituent released from activated platelets, possibly playing a variety of physiological and pathophysiological roles

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Igarashi Y. , Yatomi Y.

nr 2

We have found that sphingosine 1-phosphate (Sph-1-P) acts as an autocrine stimulator of platelets, being abundantly stored in platelets and released extracellularly, and that its exogenous addition induces platelet activation (Yatomi et al., Blood 1995, 86, 193-202) through a specific receptor on the platelet surface (Yatomi et al., J. Biol. Chem. 1997, 272, 5291-5297). Very recently, we identified Sph-1-P as a normal constituent of human plasma and serum. Sph-1-P levels in plasma and serum were 191±79 and 484±82 pmol/ml (mean ±S.D., n = 8), respectively. Platelets are most likely the source of Sph-1-P discharged during blood clotting, since they abundantly store Sph-1-P as compared with other blood cells, and release considerable amounts of stored Sph-1-P extracellularly upon stimulation. The Sph-1-P released from activated platelets may be involved in a variety of physiological processes, including thrombosis, atherosclerosis, and wound healing. Moreover, we often observed that Sph-1-P injection into mice (iv., 10 mg/kg) caused immediate rigor and death. This may be related to the recent observations from an other laboratory that nanomolar concentrations of Sph-1-P affected atrial myocyte K+ channel. These observations taken together strongly suggest pathophysiological roles of the released Sph-1-P in the blood. As one example, we found that Sph-1-P content in the plasma of platelet concentrates correlated with poor platelet increments after transfusion and with the occurence of transfusion reactions in patients.