ELUCIDATION OF ANTITHROMBOGENIC MECHANISM ON PHEMA-PST-PHEMA ABA TYPE BLOCK COPOYMER SURFACE WITH LAMELLAR SHAPED-MICRODOMAIN STRUCTURE

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In order to elucidate the antithrombogenic mechanism on PHEMA-PSt-PHEMA ABA type block copolymer surfaces (HSB) with lamellar shaped-microdomain structure, ultrastructures of platelet membrane glycocalyx (GC) and membrane skeleton (MS) -dissociated and MS-non-dissociated platelets that adhered to the HSB surfaces were analyzed by transmission electron microscopy (TEM). The number of storage granules per 1mum^2 of MS-non-dissociated and MS-dissociated platelets was then evaluated quantitatively by the image processor-analyzer. PSt and PHEMA-PSt random copolymer (HSR) surfaces were used as controls. The interaction of the platelets and the control polymer surfaces was carried out with the microsphere column method under the different flow rate conditions. The platelet GC was stained with ruthenium red. The dissociation of platelet MS was treated with dibucaine hydrochloride. The platelets on the HSB surfaces adhered with supporting narrow spaces which formed scaffolding, keeping the GC t … More he same as the intact platelet GC.On the other hand, the platelets on the control polymer surfaces adhered without the narrow spaces for the GC,indicating strong adhesion. Their external GC seemed to be lacked in some places. The ultrastructural changes of MS-non-dissociated platelets on the HSB surfaces were inhibited significantly compared to that on the control polymer surfaces. The number of the platelet storage granules on the HSB surfaces did not indicate any significant difference compared to those of the intact platelets. On the other hand, the MS-dissociated platelets adhered to all the control polymer surfaces were observed to form round shapes. The number of the platelet storage granules did not indicate any signifficant difference between all the polymer surfaces and the intact platelets. It was suggested that the microdomain structure of the HSB surfaces inhibited the ultrastructural changes by obstructing the transmembrane signaling to the MS from the GC without regard to the different flow rates. Less