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Hindi Magnesium sulfate as an analgesic in the inflammatory pain - preclinical findings
Dragana Srebro
University of Belgrade, Serbia
: Analg Resusc: Curr Res
Abstract
Adjuvant analgesics are commonly used in the treatment of chronic painful conditions. Magnesium is recognized to antagonize N-methyl-D-aspartate (NMDA) receptor channels and block calcium influx. Magnesium has been demonstrated analgesic efficacy against neuropathic pain, but data on the inflammatory pain are few and controversial.It enhances the analgesic effects of opioids, general and local anesthetics. We investigated whether magnesium sulfate affects somatic and visceral inflammatory pain and whether antinociceptive doses of magnesium sulfate cause motor impairment and/or sedation. Male Wistar rats were used. In a model of carrageenan-induced mechanical hyperalgesia magnesium sulfate had no effect when injected locally into the inflamed paw. However, subcutaneous magnesium sulfate, given in the pretreatment (before induction of inflammation) at doses of 0.5-30 mg/kg, reduced the hyperalgesia by 24.6±7 to 68±8%. Magnesium sulfate at doses of 5 and 30 mg/kg given as a treatment (2h after the induction of inflammation) produced anti-hyperalgesic effect of 43.7±6 and 27.3±4%, respectively. In acetic acid-induced writhing test magnesium sulfate given subcutaneously at doses of 1-15 mg/kg decreased the number of writhing by 49.8±10 to 77.4±2%. Higher doses of magnesium sulfate did not affect the number of writhing. In both models of pain magnesium sulfate demonstrated analgesic effect in a dose-independent manner. In a rotarod test, magnesium sulfate did not disturb motor performance in rats. Considering a therapeutic perspective, magnesium sulfate may be useful analgesics in the management of somatic and visceral inflammatory pain, at doses that do not induce motor impairment. Magnesium sulfate is effective against somatic inflammatory pain after systemic, but not after local peripheral administration. Systemic magnesium sulfate has anti-hyperalgesic effect in both the early and late phase of inflammation.
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