本研究主要是利用在多孔性高分子膜表面，血漿蛋白質吸附與血小板貼附，與此兩者之間的相互關係，配合膜的親疏水性進行討論，以期能說明多孔膜的生體適應性，以及血漿中蛋白質吸附至多孔膜表面時，可能對血小板貼附所造成的影響。第一個部份為靜態地吸附蛋白質與血小板，並利用單一蛋白質在多孔膜上吸附後，對血小板貼附的影響；第二個部份則是進行多孔膜接觸血漿，在不同時間長短下的蛋白質吸附檢測，並在不同時間吸附蛋白質後進行血小板的貼附實驗。 在靜態蛋白質吸附實驗中，利用自配製之三種血漿主要蛋白質混合液(fibrinogen、human serum albumun與?-globulin)與離心全血後所得血小板貧乏血漿(PPP)進行蛋白質吸附，因蛋白質的競爭性吸附，與血漿中其他分子對蛋白質的取代作用(Vroman effect)，故在兩種溶液中的蛋白質吸附量，除了容易改變構型與表面作用力較強的fibrinogen之外，並無明顯相關性。血小板吸附實驗則是以離心全血後得富含血小板溶液(PRP)，貼附後以掃瞄式電子顯微鏡(SEM)，觀察血小板的表面形貌與計數貼附量，而比較其與蛋白質吸附的結果，血小板的貼附量與fibrinogen吸附量呈一線性關係；另外在經過單一蛋白質吸附後，進行移除血漿蛋白質後所得之無血漿血小板溶液(serum-free platelet, SFP)的貼附，也可發現 fibrinogen對血小板貼附有正面的影響，因為血小板表面具有糖蛋白(GPIIb/IIIa)，是為與fibrinogen結合的受器。 而隨時間進行的實驗，利用PPP進行吸附便可清楚觀察到，在平坦的玻璃蓋玻片表面上，蛋白質的吸附符合競爭性吸附的描述，但在表面呈纖維狀，較不平坦的多孔膜則無此現象。而在PPP隨時間吸附後進行SFP中血小板的貼附，觀察到在多孔膜上仍然會有血小板貼附達最大值後，隨時間減少的情形，與蛋白質吸附量量測的結果不同，推測原因為蛋白質在吸附於多孔膜表面後，發生了構型重排，雖保有被特定抗體專一辨識的性質，但已失去與血小板產生連結的功能。 Surface properties of poymeric biomaterials, such as specific functional groups, charges, and hydrophobicity, play important roles in modulating protein adsorption and cell adhesion on polymeric membranes. Besides, the competitive nature of protein adsorption makes the adsorption behavior and the induced cell adhesion complex. The competitive adsorption of proteins depends upon its molecular weight, bulk concentration of proteins and surface affinity to the proteins. The major focus of this study is to investigate the influencing factors for plasma protein adsorption and platelet adhesion on the membrane filters having various kinds of chemical structure and pore size. We found that the adsorption amounts of fibrinogen and ?-globulin decreased while increase of that of human serum albumin (HSA) increased with the membrane hydrophobicity increasing. The human serum albumin was more adsorbed on the membranes from platelet-poor-plasma (PPP) than from mixed protein solution (MPS) consisting of human albumin, ?-globulin and fibrinogen. This tendency was extensively found on hydrophobic membranes compared to the hydrophilic membranes. The number of adhering platelets was lower on membranes with a decreased amount of adsorbed fibrinogen. Suppression of platelet adhesion could be elucidated by a reduction of protein adsorption, in particular of fibrinogen, which bound to the platelet membrane glycoprotein, GP IIb–IIIa. Time-dependent adsorption of fibrinogen indicates that Vroman effect, the displacement of fibrinogen, induced on the flat surface such as glass plates, but was not observed on the porous polymeric membranes.
