Nitric Oxide Synthase-Independent Generation of Nitric Oxide in Rat Skeletal Muscle Ischemia-Reperfusion Injury

Nitric Oxide and Skeletal Muscle Reperfusion Injury: Current Controversies (Research Review)

“…In this way, NO levels may be determined in reperfused skeletal muscle. After 2 h ischemia in a rodent model, nitroso-haem complexes were detected in muscle only after 24 h of reperfusion, but not at the earlier stages, after 3 min, 3 h or 8 h of reperfusion [62]. This result may be interpreted in two ways; after 24 h, NO production may either be greatly increased late in reperfusion, or alternatively, levels of nitroso-haem complexes could steadily accumulate and only be detectable at 24 h reperfusion.…”

Therapeutic Interventions Against Reperfusion Injury in Skeletal Muscle

“…However, the ability of eNOS to generate NO in the ischemic tissue is compromised because of the requirement for oxygen as a substrate. As a result, NO is deficient in ischemic tissue and in the early phase of reperfusion [91][92][93]. Using our rat skeletal muscle model [24], we have also demonstrated that local intra-arterial infusion of nitroprusside (an endothelium-independent vasodilator and a donor of NO), but not acetylcholine (an endothelium-dependent vasodilator) during early reperfusion significantly prevented reperfusioninduced microcirculatory alterations and improved microvascular blood flow.…”

Ishemia-Reperfusion enhances GAPDH nitration in aging skeletal muscle

“…Nitric oxide has been reported to increase in I/R injury although the timing and duration of the increase vary with experimental conditions [3, 13-15]. While at specific concentrations nitric oxide may be a protective factor in certain tissue stress signaling processes, excess nitric oxide can be detrimental [12, 16].…”