The function of a hydrogen peroxide-detecting electroenzymatic glucose electrode is markedly impaired in human sub-cutaneous tissue and plasma

• Published in: Biosensors & bioelectronics 1993, Vol.8 (9), p.473-482
• Main Authors: Kerner, Wolfgang, Kiwit, Martin, Linke, Burkhard, Keck, Fritz S., Zier, Horst, Pfeiffer, Ernst F.
• Format: Article
• Language: English
• Subjects: Adult; Animals; Biosensing Techniques; Blood Glucose - analysis; Buffers; Connective Tissue - chemistry; Diabetes Mellitus, Type 1 - blood; Diabetes Mellitus, Type 1 - metabolism; enzyme electrode; Evaluation Studies as Topic; Female; Glucose - analysis; glucose oxidase; glucose sensor; Humans; Hydrogen Peroxide; implantation; Male; Monitoring, Physiologic - instrumentation; Prostheses and Implants; subcutaneous tissue
• ISSN: 0956-5663; 1873-4235
• DOI: 10.1016/0956-5663(93)80032-K

Electroenzymatic glucose sensors implanted into sub-cutaneous (s.c.) tissue of human subjects and experimental animals exhibit lower sensitivities to glucose than in buffer solutions before implantation. The mechanism of the decrease of sensitivity is not known. Sensors used in this study were fabricated from platinum wires (diameter 0.125 mm) with covalently bound glucose oxidase at the tip of the wire. After coating the tip with polyurethane, wires were placed into 27 gauge steel needles. Sensors were operated potentiostatically at 700 mV against Ag/AgCl pseudo-reference electrodes. These sensors were implanted s.c. in 6 diabetic patients for 7 h. In 4 patients, sensors were responsive to successive increases of plasma glucose levels. Mean sensitivity to glucose in s.c. tissue was 29% of in vitro sensitivity. In 2 patients there was a sudden decrease of sensor currents, unrelated to glucose, shortly after implantation. Sensors were inhibited in human plasma to a similar extent. When sensors were exposed to native plasma and to plasma ultrafiltrate (mol. wt. 12 kDa) caused much less decrease of sensor signals. Losses of sensor sensitivities to glucose in s.c. tissue and in plasma were totally reversible upon re-exposure of sensors to buffer solutions. We conclude that sensor inactivation in plasma and possibly in s.c. tissue is caused by low molecular weight substances not retained by the polyurethane membrane.