BOLUS METOCLOPRAMIDE DOES NOT ENHANCE MORPHINE ANALGESIA AFTER CESAREAN-SECTION

Intravenous metoclopramide potentiates the analgesic effects of opioid s in postoperative patients. We speculate that increased spinal concen trations of acetylcholine from metoclopramide-induced acetylcholineste rase inhibition is the mechanism responsible for enhanced morphine ana lgesia from metoclopramide. Sixty patients undergoing elective cesarea n section with subarachnoid anesthesia were randomized to receive eith er 20 mg metoclopramide or saline intravenously 30-60 min prior to sub arachnoid injection. Prior to subarachnoid injection of local anesthet ic, 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 an algesia, and at discharge from the postanesthesia care unit. Total mor phine use was recorded in the recovery room and for 24 h postoperative ly. There were no significant differences in VAS scores, morphine use, or CSF cholinesterase activity between groups. CSF cholinesterase act ivity was similar to values in nonpregnant patients demonstrated previ ously. This study failed to confirm the morphine-enhancing action of 2 0 mg intravenous metoclopramide in postoperative patients. Furthermore , this dose of metoclopramide does not inhibit CSF acetylcholinesteras e.