THE FUNCTION OF A HYDROGEN PEROXIDE-DETECTING ELECTROENZYMATIC GLUCOSE ELECTRODE IS MARKEDLY IMPAIRED IN HUMAN SUB-CUTANEOUS TISSUE AND PLASMA

Electroenzymatic glucose sensors implanted into sub-cutaneous (s.c.) t issue of human subjects and experimental animals exhibit lower sensiti vities to glucose than in buffer solutions before implantation. The me chanism of the decrease of sensitivity is not known. Sensors used in t his study were fabricated from platinum wires (diameter 0.125 mm) with covalently bound glucose oxidase at the tip of the wire. After coatin g the tip with polyurethane, wires were placed into 27 gauge steel nee dles. Sensors were operated potentiostatically at 700 mV against Ag/Ag Cl 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 glu cose in s.c. tissue was 29% of in vitro sensitivity. In 2 patients the re was a sudden decrease of sensor currents, unrelated to glucose, sho rtly after implantation. Sensors were inhibited in human plasma to a s imilar extent. When sensors were exposed to native plasma and to plasm a ultrafiltrate (mol. wt. <10 kDa) for 10 h, identical decreases of si gnals were found. Exposure to dialysed plasma (mel. wt. >12 kDa) cause d 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 i nactivation in plasma-and possibly in s.c. tissue is caused by low mol ecular weight substances not retained by the polyurethane membrane.