Microelectromechanical systems (MEMS) create an opportunity for the development of smaller, cheaper, and more precise biomedical instrumentation and devices. Little is known, however, about the hemocompatibility of the materials used to fabricate these devices. Because of the potentially harmful consequences of thrombus formation, a better understanding of blood interactions with bioMEMS materials is desirable. This study is an in vitro assessment of the hemocompatibility of silicon (Si), silicon dioxide (SiO2), silicon nitride (Si3N4), low-stress silicon nitride (Si(1.0)N(1.1)), SU-8 photoresist, and parylene thin films. A polycarbonate-based polyurethane, was used as a reference material. Experiments were carried out to detect differences in platelet adhesion or morphology after contact with these materials under static conditions. Platelet adhesion on Si, Si3N4, Si(1.0)N(1.1,) and SU-8 photoresist was significantly greater (P < 0.05) than platelet adhesion on polyurethane. Adhesion on parylene and SiO(2) was not significantly different from on polyurethane (P < 0.05). The median platelet area and circularity were higher on polyurethane than all other materials. Materials that showed higher levels of platelet adhesion tended to have platelets that showed less spreading, except for SiO2, where platelets exhibited relatively low adhesion and spreading. This data suggests that Si, Si3N4, Si(1.0)N(1.1), and SU-8 photoresist may be more reactive to platelets and therefore more thrombogenic than parylene, SiO2, and polyurethane. These results may be helpful in guiding the selection of materials for use in the development of blood-contacting microelectromechanical systems.

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Administration of phentermine (Phen) together with (+/-) fenfluramine (Fen) enhances the weight reduction that is observed with either drug alone; consequently, these anorectic agents are commonly prescribed together for weight reduction. Repeated administration of Fen is known to cause long-term depletion of axonal serotonin (5-HT) and loss of 5-HT transporters, and is therefore considered neurotoxic. We now report that combined administration of Phen/Fen (5 mg/kg/3.125 mg/kg, and 20 mg/kg/3.125 mg/kg) can enhance the neurotoxic effect of Fen (3.125 mg/kg) and Phen (5 mg/kg and 20 mg/kg) on central 5-HT systems. Rats were repeatedly treated once each hour for a total of four injections with saline, Phen (5 mg/kg and 20 mg/kg), Fen (3.125 mg/kg and 12.5 mg/kg), or combined Phen/Fen (5 mg/kg/3.125 mg/kg and 20 mg/kg/3.125 mg/kg), and sacrificed either 7 or 28 days after cessation of treatment. Combined administration of Phen/Fen (5 mg/kg/3.125 mg/kg and 20 mg/kg/3.125 mg/kg) caused significantly greater reductions of 5-HT levels in the striatum, nucleus accumbens/olfactory tubercle, hypothalamus, amygdala, frontal parietal cortex, and hippocampus than either drug alone. Combined Phen/Fen at the higher drug-dose combination (20 mg/kg/3.125 mg/kg) was observed to reduce the density of 5-HT transporters in rat striatum at both 7 and 28 days after cessation of treatment. In addition, combined administration of Phen/Fen (5 mg/kg/3.125 mg/kg and 20 mg/kg/3.125 mg/kg) caused greater weight loss than that observed with either compound alone. Collectively, the present data demonstrate that combined Phen/Fen administration enhances the neurotoxicity of Phen or Fen on 5-HT neurons.

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