Intrauenous Magnesium Sulfate Administration Reduces Propofol Infusion Requirements during Maintenance of Propofol-N2O Anesthesia

Abstract

THE magnesium ion blocks the ion channel of the N -methyl-d-aspartate (NMDA) receptor in a voltage-dependent fashion. 1 Also, increased extracellular magnesium concentrations in vitro cause a noncompetitive NMDA blockade. 2 Several studies have shown that intrathecal administration of magnesium sulfate alone produced a small degree of antinociception or no antinociception but resulted in potentiated antinociception when magnesium was coadministered intrathecally with morphine. 3,4 Our recent work has demonstrated that magnesium sulfate potentiated the analgesic effect of bupivacaine when coadministered intrathecally with bupivacaine in rats. 5 Also, some studies have reported that perioperative administration of intravenous magnesium sulfate reduced intra- and postoperative analgesic requirements in patients undergoing arthroscopic knee surgery or elective abdominal hysterectomy. 6,7 In one of the studies, when the propofol infusion rate was held constant and the fentanyl dose was adjusted to hemodynamic endpoints, opioid requirements were reduced. 6 This result suggests that the effect of magnesium on anesthesia should be studied further. Accordingly, we investigated whether intravenous administration of magnesium sulfate reduces propofol infusion requirements during maintenance of propofol–N2O anesthesia.