Unraveling the Complexity of Polyurethane Hemocompatibility

The hemocompatibility of materials used in biomedical applications is crucial, especially when those materials come into contact with blood. Recent research has highlighted the role of albuminated polyurethane (PU) surfaces in reducing thrombogenicity by masking these surfaces from the host defense mechanisms activated by blood. Studies suggest that these albumin-coated surfaces demonstrate lower thrombogenic potential, which is essential for improving patient outcomes in scenarios involving blood contact.

In addition to albumin, other strategies to enhance the hemocompatibility of polyurethanes have been explored. Modifications to polymer surfaces, such as the incorporation of polyethylene oxide (PEO) chains, poly(vinyl pyrrolidone), or negatively charged sulfonate groups, have shown promise in reducing plasma protein adsorption. This reduction appears to correspond with decreased bacterial adhesion, which is beneficial for minimizing the risk of infection in implanted devices.

The interaction between biomaterials and inflammatory cells is another area of significant interest. Research indicates that the inflammatory response at the tissue-implant interface is governed by the interactions between blood proteins and various immune cells. Notably, studies have revealed that precoating materials like Biomer™ with albumin can enhance monocyte activation, leading to increased interleukin-1 (IL-1) secretion, while other proteins—such as fibrinogen and IgG—have a less pronounced effect on this activation.

Conversely, surface treatments with albumin have been shown to mitigate monocyte activation, highlighting a potential strategy for reducing inflammatory responses. For instance, a study found that treating Pellethane™ 2363, a commonly used PU in medical devices, with albumin resulted in lower IL-8 secretion from monocytes, suggesting that this treatment could help prevent thrombotic complications when devices are initially placed in circulation.

The findings underscore the intricate balance between the advantages and disadvantages of protein adsorption on biomedical polymers. While albumin may effectively minimize platelet and bacterial adhesion, it can also inadvertently activate inflammatory pathways that inhibit cellular activities essential for healing. Thus, the relationship between blood, proteins, and polymer surfaces is complex, and ongoing research aims to elucidate these interactions further to enhance the design of future biomedical materials.