Abstract

BackgroundMagnesium has been proven to have antinociceptive effects in animal and human models of pain. Its effect is primarily based on the regulation of calcium influx into the cell, which is natural physiological calcium antagonism and N-methyl-d-aspartate (NMDA) receptor antagonism. MethodsOne hundred and eight patients undergoing surgery with spinal anesthesia received either 250 mg of intravenous magnesium sulfate followed by an infusion of 500 mg magnesium sulfate (25 mg/mL) at the rate of 20 mL/hour; or the same volume of normal saline (control group) as bolus and infusion. The primary end-points in the study were to evaluate the analgesic effect and duration of sensory and motor blockade. The secondary end-points included assessment of hemodynamic effects of intravenous magnesium sulfate and rescue analgesia requirement. ResultsSensory and motor blockade, respectively, were 25 minutes and 34 minutes shorter in the control group. Less patients in the magnesium group (33% vs. 53.7%) than in control group required rescue analgesia in the postoperative period. The control group required rescue analgesia nearly 3 hours earlier than the magnesium group. Only one patient in the control group experienced bradycardia. There was no event of intraoperative hypotension in either of the groups. ConclusionIntravenous magnesium sulfate when given as a bolus, followed by an infusion, delayed and decreased the need of rescue analgesics after spinal anesthesia.

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