Understanding spontaneous output fluctuations of an amperometric glucose sensor: effect of inhalation anesthesia and use of a nonenzyme containing electrode.

Implantable glucose sensors are often unstable in vivo. Possible causes include local oscillations of glucose or oxygen levels, fluctuation of interferants, and external electromagnetic interference. To better understand glucose versus nonglucose mediated fluctuations, we compared sensors fabricated with glucose oxidase versus blank electrodes without enzyme in rabbits. We also investigated the effect of general anesthesia. We used power spectral analysis to investigate transmitted signals from amperometric peroxide sensing devices 2-3 weeks after subcutaneous implantation. Fasted animals were studied for 90 minutes in the conscious state and for 90 minutes during halothane anesthesia. Animals exhibited almost no body movement during the studies. In the conscious state, enzyme active sensors demonstrated more oscillations than blank electrodes at almost all frequencies from 2 to > 8 cycles per hour. This finding suggested that the spontaneous fluctuations were secondary to local changes in glucose or oxygen. Because fluctuations were not seen in the blank electrode, periodic changes in interferant concentrations, electromyographic activity, or in external electromagnetic interference are unlikely. General inhalation anesthesia was associated with markedly reduced sensor output fluctuation at almost all frequencies in enzyme active sensors. We conclude that fluctuation of electrochemical glucose sensor output, unrelated to fluctuations in blood glucose, is likely secondary to spontaneous changes in the local concentration or vascular delivery of glucose or oxygen. Anesthesia may have stabilized blood flow, preventing normal spontaneous autoregulatory variation.