Oxygen tension at the subcutaneous implantation site of glucose sensors.

To elucidate potential influences of the average tissue pO2 on the function of implanted glucose sensors, non-miniaturized polarographic oxygen electrodes and glucose oxidase/H2O2 glucose electrodes were implanted in the subcutaneous tissue of spontaneously breathing normal and diabetic dogs. There was no appreciable run-in phenomenon of oxygen sensors but normally a pronounced initial decrease in current after implantation of glucose sensors. The subcutaneous pO2 amounted to an average of 7 kPa in air-breathing animals with no difference between normal and insulin-dependent diabetic dogs. It showed oscillations of approximately +/- 2 kPa but the mean was stable over the maximum duration of experiments of 16 h. Induced alterations of tissue pO2 between less than 2 and greater than 20 kPa (as verified by measurements of arterial pO2) were not followed by alterations in the current of nearby implanted glucose sensors. It is concluded that the frequently observed instabilities and losses in sensitivity of the system "implanted glucose sensor in situ + tissue glucose compartment" are not caused by alterations in tissue pO2.