Biocompatibility

All the biochemical monitoring techniques described above have shown eliability and efficacy in vitro. Unfortunately, the complexities of human plasma, with platelets, plasma proteins, and the clotting cascade, and problems with biocompatibility have made their application in vivc unreliable. This has limited application to research designs or short (hours) clinical utility. Plasma protein adherence, platelet adherence, and coagulation protein adherence have all led to ineffective sensor function. Extensive investigation is now focusing on ways of improving the hemocompatibility of invasive sensors.

Exposure of an irregular polymer or fiber-optic surface leads to rapid absorption of various proteins and platelet adherence. Placing a negative charge on the surface will tend to diminish adherence of the large negatively charged plasma proteins. Covalent bonding of heparin limits platelet adhesion and deactivates coagulation enzymes such as thrombin. Albumin coating will also reduce platelet adhesion ( BenmakrohaeLa/ 1995).

All these approaches have been attempted with mixed success. None provides the protection needed to maintain proper sensor function and minimize risk to the biological system over a suitable length of time. The latest attempts at improving biocompatibility have been in cell membrane mimicry. Synthesized biomembrane copolymers have been developed which mimic the thrombosis-resisting properties of the relatively inert red blood cell membrane ( Rolfe 1995). However, this technology is still in its infancy, and will require much further improvement before it is clinically applicable.

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