Qu R, Furukawa N, Fukuda H
Department of Physiology, Kawasaki Medical School, Kurashiki, Japan.
J Auton Nerv Syst. 1995 Dec 5;56(1-2):87-96. doi: 10.1016/0165-1838(95)00061-0.
To investigate changes in motility of the extrahepatic biliary system associated with emesis, we measured the volume of the gallbladder and flow resistance through the sphincter of Oddi, as well as antral and duodenal contractilities before and during retching in decerebrate paralyzed dogs. Motilities of the gallbladder, sphincter of Oddi, duodenum and antrum were enhanced with most episodes of fictive retching elicited by stimulation of the central part of the severed dorsal, as well as the ventral trunk of the thoracic vagus nerve. These enhanced motilities persisted until the end of retching. Motilities of the sphincter of Oddi and duodenum were sometimes transiently depressed at the beginning of retching. This depression in the sphincter continued for only 13 +/- 1.0 s, while the gallbladder contraction continued for 65 +/- 3.4 s. Motilities were rarely enhanced by vagal stimulation when retching was not elicited. These changes in motilities were abolished by bilateral vagotomy. The serum gastrin level was increased just after and 10 min after retching only when the ventral vagal trunk remained intact, while the plasma cholecystokinin level was not changed with retching. These results suggest that bile evacuation is interrupted with emesis despite contraction of the gallbladder during retching, since the sphincter of Oddi also contracts simultaneously.
