Gastroenterology · 1984
Influence of transsphincteric fluid flow on spike burst rate of the opossum sphincter of Oddi.
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Takahashi I, Dodds W J, Itoh Z, Hogan W J, Kern M K
Аннотация
In this study, we evaluated the effect of transsphincteric fluid flow on the rate of spike bursts in the opossum sphincter of Oddi (SO). For chronic studies in awake animals, bipolar electrodes were implanted on the SO, gastric antrum, duodenum, and jejunum. In group 1 animals, surgery was limited to electrode implantation. Subsequently, these animals underwent a cholecystectomy. Group 2 animals had electrode implantation without further surgery. In group 3 animals, bile flow was diverted around the SO, whereas in group 4 animals, pancreatic juice as well as bile was diverted around the SO. Multiple myoelectric recordings were obtained in each animal during fasting and after feeding. In fasted control animals, the rate of SO spike bursts showed cyclic increases synchronous with phase III of the duodenal migratory myoelectric complex. Feeding increased the rate of SO spike bursts. Cholecystectomy had no effect on SO spike bursts in fasted animals. Diversion of bile or bile and pancreatic juice around the SO did not alter the fasting pattern of SO spike bursts. However, flow diversion in the group 3 and group 4 animals did cause a modest decrease of SO spike bursts, from approximately 2/min to about 1/min, during phase I of the duodenal migrating myoelectric complex (p less than 0.05). Sphincter of Oddi spike-burst rate was not affected during the remainder of the migrating myoelectric complex cycle. Neither cholecystectomy nor flow diversion caused any change in the normal SO responses to feeding. Excitatory SO responses caused by motilin or by cholecystokinin-octapeptide were shown to be independent of changes in transsphincteric flow. We conclude that variations in transsphincteric flow cause only minimal alteration of the rate of spike bursts in the opossum SO during fasting. Therefore, factors other than transsphincteric flow, such as hormonal or neural influences, appear to be the major mechanism(s) that regulate the rate of SO contractions in awake opossums.