AJP - Gastrointestinal and Liver Physiology, Vol 257, Issue 1 41-G45, Copyright © 1989 by American Physiological Society
Regulation of plasma motilin by opioids in the dog
P. Poitras, M. Boivin, R. G. Lahaie and L. Trudel
Andre-Viallet Clinical Research Center, Hopital Saint-Luc, University of Montreal, Quebec, Canada.
In the first part of this study, we compared the effects of morphine and
trimebutine, two opioid receptor agonists, on small intestinal motility and
plasma motilin in dogs. Morphine (100 micrograms/kg iv for 10 min) induced
first a typical vomiting myoelectric profile followed subsequently by a
migrating electrical activity mimicking phase III of the migrating
myoelectric complex; trimebutine (5 mg/kg iv for 10 min) initiated only a
migrating phase III-like activity. Despite their different initial
contractile effects, both agents induced a significant and similar rise in
plasma motilin that preceded the beginning of the premature phase III. In
the second portion of the study, naloxone, an opioid receptor antagonist,
was infused to verify the influence of endogenous opiates on plasma motilin
and on the migrating motor complex. Naloxone (2 mg/kg, then 0.5 mg.kg-1.h-1
iv) delayed significantly the cyclic recurrence of plasma motilin peak
increases and of the phase IIIs. In some animals, where naloxone abolished
the phase IIIs, the amplitude of the motilin peak increases was
significantly diminished. These results suggest 1) that opioid
administration increases plasma levels of motilin by a mechanism that is
independent of the intestinal contractile activity, and 2) that endogenous
opioids could be physiological inducers of plasma motilin increases in the
conscious dog.
