Driver_1996_Anesth.Analg_82_1033

Intravenous metoclopramide potentiates the analgesic effects of opioids in postoperative patients. We speculate that increased spinal concentrations of acetylcholine from metoclopramide-induced acetylcholinesterase inhibition is the mechanism responsible for enhanced morphine analgesia from metoclopramide. Sixty patients undergoing elective cesarean section with subarachnoid anesthesia were randomized to receive either 20 mg metoclopramide or saline intravenously 30-60 min prior to subarachnoid injection. Prior to subarachnoid injection of local anesthetic, 2 mL of cerebrospinal fluid (CSF) was aspirated for cholinesterase activity measurement. Visual analog scale (VAS) scores for pain were obtained prior to drug administration, at first patient request for analgesia, and at discharge from the postanesthesia care unit. Total morphine use was recorded in the recovery room and for 24 h postoperatively. There were no significant differences in VAS scores, morphine use, or CSF cholinesterase activity between groups. CSF cholinesterase activity was similar to values in nonpregnant patients demonstrated previously. This study failed to confirm the morphine-enhancing action of 20 mg intravenous metoclopramide in postoperative patients. Furthermore, this dose of metoclopramide does not inhibit CSF acetylcholinesterase.