Nitric oxide in ischemic and reperfused human muscle.

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. We also measured cytochrome oxidase activity and malondialdehyde (MDA).

Results: NO increased during ischemia but it soon returned to normal values upon reperfusion. On the other hand, cytochrome oxidase that also decreased in ischemic muscle did not increase during the reperfusion and malondialdehyde only increased during reperfusion, indicating the occurrence of peroxidative reactions in this situation.

Conclusions: NO is implicated in the ischemia/reperfusion pathology, but it is difficult to relate whether this is connected to cytochrome oxidase activity and malondialdehyde formation, also modified in this ischemia-reperfusion model.