The potentiation or prolongation by propanidid of the neuromuscular block induced by suxamethonium has been previously noted 1. The prolongation of suxamethonium apnoea has also been documented objectively 1 * 2.The aim of this study was to examine quantitatively and qualitatively the interaction between propanidid and the two depolarising neuromuscular blocking agents, suxamethonium and decamethonium. METHODThe study was performed on 45 consenting adult patients about to undergo elective surgery not requiring profound peripheral relaxation. Subjects had no known disease of the cardiovascular or respiratory systems or of the neuromuscular junction. They were heavily premedicated with a narcotic analgesic and a belladonna alkaloid, frequently supplemented by droperidol. Anaesthesia was induced with thiopentone followed by nitrous oxide, oxygen and halothane. The larynx and glottis were sprayed with lignocaine and, after anaesthesia had been deepened, an endotracheal tube was passed. The subjects were then positioned for surgery with one arm taped m y to a special arm-board. Apnoea was induced by moderate hyperventilation and the subjects were then connected to a constant volume ventilator and ventilated at a constant rate and volume throughout the study. Anaesthesia was maintained with 0.5 to 1.0 per cent halothane. The blood pressure was checked frequently.Square wave pulses (0.2ms) were applied to the ulnar nerve at the wrist through 24 SWG subcutaneous electrodes with a Grass S4G stimulator every ten seconds. The voltage was adjusted to double that required to produce a maximal contraction of the adductor pollicis. The pulse duration and voltage were monitored on a Tectronix 546 oscilloscope. The force of contraction of the adductor pollicis was measured with a Grass FT 03 force-displacement transducer, the output of which was recorded on a Grass 5D polygraph.