The blood compatibility of biomaterials is an important condition for the application of medical devices. Although systemic anticoagulation can be used to address inferior hemocompatibility of materials and devices, the adverse effects make materials with superior hemocompatibility highly desirable, especially for long-term use.
Alfa Chemistry has conducted extensive research to modify the surface properties of biomaterials to enhance their hemocompatibility. Our chemical surface modification research and applications have been fruitful. If you would like to quickly modify the surface of your material for biomedical applications, please contact us.
Alfa Chemistry's research aims to define hemocompatibility profiles of biomaterial surfaces, which will lead to the design of blood-compatible material surfaces using knowledge-based design. Hemocompatibility refers to a biomedical implant's capacity to interact with the body's circulating blood, i.e., medical devices that can come into direct contact with blood without causing unwanted side effects. The design and operation of the device in the blood, as well as coagulation biochemistry and surface-blood interactions, all influence this aspect. In the biomaterial-blood compatibility process, the coagulation cascade reaction, complement system, platelets, and leukocytes are generally divided into four important processes. Given these considerations, the surface modification tactics we utilize to combat protein contamination and platelet adhesion can also be used to improve hemocompatibility, at least to some extent.
Fig 1. (A) Thrombus formation around the heart valve frame and strut. (B) Fibrin formation and (C) fibrin with thrombus formation. (Manivasagam V. K, et al. 2021)
Alfa Chemistry is familiar with the interaction of blood components with foreign biomaterials as well as the material's surface properties and can create hemocompatible biomaterials for customers upon request. Surface passivation, bioactive molecule functionalization, and endothelialization are all strategies for creating hemocompatible surfaces.
Surface modification by Alfa Chemistry through coating or through physical or chemical functionalization of biomaterial surfaces plays a key role in the prevention of these complications. Modifications to resist blood protein adsorption and cell adhesion, as well as active suppression of the coagulation cascade and platelet activation, are all used to create hemocompatible surfaces. A distinction between passive and active surfaces can be made in general. Bioactive surfaces interact directly with blood components, whereas passive or biologically inert surfaces operate as a barrier between foreign biomaterials and blood.
Hydration and steric repulsion are exploited by repelling surface charges, fabricating superhydrophilic surfaces, and layers of hydrophilic macromolecules to alter surface properties to reduce interfacial energies that promote protein adsorption and create repulsive barriers.
|Inorganic Coating||Inorganic modifications such as metal oxides, metal nitrides and carbon-based coatings|
Diamond-like carbon (DLC) coatings, boron-carbon-nitrogen coatings, pyrolytic carbon films.
These coatings are manufactured by chemical vapor deposition and are used in medical devices.
|Organic Coating||Surface modifications with organic molecules to control protein and cell interactions with surfaces include incorporation of brush-forming polymers and zwitterionic polymers and the use of passivating albumin layers.|
|Textured Surfaces||There are several methods to modify the surface topography and create textured surfaces, including the preparation of micropatterns on titanium oxide layers using sintered titanium or argon plasma etching, solvent casting of PU, etc.|
Biological active surfaces can be an effective method to prevent activation of coagulation or inflammation.
|Anticoagulant Surfaces||The most common method of surface modification with anticoagulants is to immobilize heparin.|
The direct thrombin inhibitor hirudin.
Anticoagulant proteins, including thrombomodulin and activated proteins.
|Platelet Inhibitors||Blood platelet inhibitors are another modification strategy to prevent thrombus formation on blood-contacting medical devices. |
Surface coatings and release systems, targeting adhesion, activation, and aggregation of platelets are based on, e.g., prostaglandin E1, dipyridamole, the immobilization of apyrase, systems eluting GPIIb/IIIa inhibitor abciximab, and nitric oxide (NO)-releasing coatings.
|Endothelialization||Reconstruct or mimic the endothelial layer to mimic the natural antithrombotic lining of blood vessels||In vitro cell seeding.|
In vivo autoendothelialization induced by endothelial progenitor cells.