Background: Biochemical events explaining the pathology of ischemia-reperfusion in the muscle are still debated. Nitric oxide (NO) has been postulated to be implicated in these phenomena, but the short half-life of this compound makes it difficult to measure.
Methods: In this paper, we used an amperometric solid-sate sensor to measure NO concentrations in frozen human muscles before, during and after a period of ischemia.