Mediation of in vivo glucose sensor inflammatory response via nitric oxide release

Raeann Gifford, Melissa M. Batchelor, Youngmi Lee, Giridharan Gokulrangan, Mark E. Meyerhoff, George S. Wilson

Research output: Contribution to journalArticlepeer-review

98 Scopus citations


In vivo glucose sensor nitric oxide (NO) release is a means of mediating the inflammatory response that may cause sensor/tissue interactions and degraded sensor performance. The NO release (NOr) sensors were prepared by doping the outer polymeric membrane coating of previously reported needle-type electrochemical sensors with suitable lipophilic diazeniumdiolate species. The Clarke error grid correlation of sensor glycemia estimates versus blood glucose measured in Sprague-Dawley rats yielded 99.7% of the points for NOr sensors and 96.3% of points for the control within zones A and B (clinically acceptable) on Day 1, with a similar correlation for Day 3. Histological examination of the implant site demonstrated that the inflammatory response was significantly decreased for 100% of the NOr sensors at 24 h. The NOr sensors also showed a reduced run-in time of minutes versus hours for control sensors. NO evolution does increase protein nitration in tissue surrounding the sensor, which may be linked to the suppression of inflammation. This study further emphasizes the importance of NO as an electroactive species that can potentially interfere with glucose (peroxide) detection. The NOr sensor offers a viable option for in vivo glucose sensor development.

Original languageEnglish
Pages (from-to)755-766
Number of pages12
JournalJournal of Biomedical Materials Research - Part A
Issue number4
StatePublished - 15 Dec 2005


  • Biocompatibility
  • Glucose sensor
  • In vivo
  • Inflammatory response mediation
  • Nitric oxide


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