Glycemia-dependent nuclear factor κB activation contributes to mechanical allodynia in rats with chronic postischemia pain.

Background: Ischemia-reperfusion injury causes chronic postischemia pain (CPIP), and rats with higher glycemia during ischemia-reperfusion injury exhibit increased allodynia. Glycemia-induced elevation of nuclear factor κB (NFκB) may contribute to increased allodynia.

Methods: Glycemia during a 3-h ischemia-reperfusion injury was manipulated by: normal feeding; or normal feeding with administration of insulin; dextrose; or insulin/dextrose.

Effects of glycemic regulation on chronic postischemia pain.

Background: Ischemia-reperfusion (I/R) injuries consist of enhanced oxidative and inflammatory responses along with microvascular dysfunction after prolonged ischemia and reperfusion. Because I/R injuries induce chronic postischemia pain (CPIP) in laboratory animals, it is possible that surgical procedures using prolonged ischemia may result in chronic postoperative pain. Glycemic modulation during ischemia and reperfusion could affect pain after I/R injury because glucose triggers oxidative, inflammatory, and thrombotic reactions, whereas insulin has antioxidative, antiinflammatory, and vasodilatory properties.