J.E. Geenen

The effects of morphine on intraluminal pressures recorded from the sphincter of Oddi (SO) at endoscopic retrograde cholangiopancreatography in 19 patients who were without evidence of biliary or pancreatic disease were studied. Morphine was given in four successive doses of 2.5, 2.5, 5, and 10 micrograms/kg iv at five minute intervals. Morphine in subanalgesic doses increased the frequency of SO phasic pressure waves to a maximum of 10-12/min, caused the phasic waves to occur simultaneously along the sphincter segment, increased phasic wave amplitude from 72 (26) (SE) to 136 (31) mmHg, and increased SO basal pressure from 10 (1) to 29 (9) mmHg (p less than 0.05). The effects of morphine on the SO are mediated by more than one opioid receptor type, as naloxone competitively antagonised the increase in phasic wave frequency induced by morphine, but did not affect the increase in SO basal pressure elicited by morphine. When given after naloxone, morphine decreased phasic wave amplitude, an inhibitory effect that is normally masked by morphine's dominant naloxone sensitive excitatory effect. Mu receptors do not appear to be involved in control of spontaneous SO motor function, as naloxone alone did not affect SO motor activity. The excitatory effects of morphine on the SO are not mediated by cholinergic nerves, as they were not blocked by atropine. Cholinergic nerves, however, may have a role in regulating spontaneous SO motor function because atropine alone depressed phasic wave activity and basal pressure. Although morphine does cause 'spasm' of the human SO, its effects are more complex than is commonly believed.

Abstract Phasic pressure waves have been recorded previously from the human sphincter of Oddi during endoscopic retrograde cholangiographic examination. However, the relationship of these waves to each other along the entire length of the sphincter of Oddi segment has not been determined. In this study we evaluated the motor activity of the sphincter of Oddi and common bile duct in 15 patients with common duct stones and 20 control patients with a normal biliary tract. Via endoscopy a triple-lumen catheter with three recording orifices spaced at 2-mm intervals was inserted into the papilla and directed into the common bile duct. Pressures were initially recorded from the common bile duct and then with all three orifices recording from within the sphincter of Oddi segment. The direction of propagation for the sphincter of Oddi phasic contractions was scored for a 3-min interval. No significant difference existed between controls and patients with common duct stones for common bile duct pressure, sphincter of Oddi basal pressure, and sphincter of Oddi phasic wave amplitude, frequency, and duration. A significant difference, however, was found in the percentage of antegrade and retrograde wave sequences between controls and patients with common duct stones, in controls 60 ± 4% of wave sequences were antegrade and 26 ± 3% were retrograde. In contrast, in patients with common duct stones 18 ± 5% of wave sequences were antegrade and 53 ± 9% were retrograde. There was no significant difference between the two groups in the percentage of simultaneous sphincter of Oddi contractions. Whether the difference in direction of sphincter of Oddi pressure wave propagation between patients with common duct stones and controls is a primary or secondary aberration of sphincter of Oddi motor function is not determined by this study. If primary, alteration of the predominant antegrade sequencing of phasic contractions normally present in the sphincter of Oddi could contribute to the retention or development of common duct stones, or both.