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AJP - Gastrointestinal and Liver Physiology, Vol 255, Issue 5 619-G626, Copyright © 1988 by American Physiological Society
ARTICLES |
T. Suzuki, W. J. Dodds, S. K. Sarna, W. J. Hogan, R. A. Komorowski and Z. Itoh
Department of Medicine, Medical College of Wisconsin, Milwaukee 53226.
Our aim in this study is to determine whether extrinsic autonomic nerves regulated spike-burst rate in the opossum sphincter of Oddi (SO) during fasting or after feeding. We implanted electrodes on the distal SO, proximal SO, gastric antrum, duodenum, and jejunum of 20 animals. A cut transection and reanastomosis was done at different levels of the SO to interrupt putative extrinsic or intrinsic nerves, or the SO was painted with phenol to impair extrinsic nerves. Like controls, animals with a cut and reanastomosis at the proximal SO or at the SO-duodenal junction showed a normal fasting pattern of cyclic changes in SO spike-burst rate. In contrast, animals treated by a distal SO cut or phenol treatment at the distal SO lost the normal cyclic pattern of SO spike bursts and had a constant rate of approximately 4/min. A cut through the middle SO uncoupled the spike bursts in the proximal and distal SO. After feeding, all animals developed an SO spike-burst rate of 5-6/min that lasted for several hours. We conclude that the normal fasting pattern of SO spike bursts is regulated by extrinsic nerves that ascend cephalad along the sphincter segment, whereas the sustained increase in SO spike-burst rate after feeding is at least in part hormonal.
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