Abstract
The effect of cholecystokinin (CCK) upon the intestinal motility has not been entirely explored in ruminants. The aim of this study was to examine the precise effects of CCK amphibian analogue, cerulein, on small-intestinal myoelectric activity in rams in the course of chronic experiments. Five rams underwent implantation of bipolar platinum electrodes to the duodenal bulb, the distal duodenum and jejunum. During continuous myoelectrical and motor recordings, 0.15 M NaCl or the various doses of cerulein were administered intravenously. Short infusions of the smallest dose of cerulein exerted a slight and mostly insignificant effect on the duodenalbulb and the duodenal myoelectric activity index (MAI) values. In the duodenal bulb, the effects of cerulein on myoelectric activity were dose-dependent and closely related to the phase of the MMC. In the duodenum, the higher doses of the hormone evoked short stimulatory response followed by longer inhibitory biphasic effects on MAI. These effects were inversely related to the duration of hormone injection. Infusions of hormones at the higher doses caused a less pronounced biphasic effect. It is concluded that cerulein exerts an inhibitory effect upon the myoelectric activity of the duodenal bulb and a strong stimulatory and inhibitory (biphasic) effect on duodenal motility in sheep.
Highlights
Duodenal motility is a very important intestinal phenomenon, crucial for normal digestion and absorption, and its motor functions are controlled by many neurohormonal mechanisms
Short infusions of the small dose of cerulein administered during phase 1 of the migrating motor complex (MMC) induced no changes, while short infusions during phases 2a and 2b of the MMC induced the weakest alterations in the spike bursts in the duodenal bulb (Table 1)
Infusions of moderate doses of cerulein inhibited spike bursts in the duodenal bulb for longer periods than after infusion of the small doses only the value obtained during phase 2b was significant when the hormone was infused over 30 s and during phase 2a and 2b when the hormone was infused over 60 s (Table 1)
Summary
Duodenal motility is a very important intestinal phenomenon, crucial for normal digestion and absorption, and its motor functions are controlled by many neurohormonal mechanisms. The role of the hormone is not limited to motility and it participates in the control of other physiological functions.[54] In humans and monogastric animals, CCK affects the motor activity of the whole gastrointestinal tract in vivo and in vitro.[2,11,56] The recognised effect of CCK on small-intestinal motility is clear. The hormone inhibits the arrival of the migrating motor complex (MMC) in the upper small bowel.[19] it evokes the specific spike burst pattern and may increase spiking activity as well as hasten intestinal transit time.[29,36,56] Its amphibian analogue, cerulein, is active in mammals.
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More From: Journal of the South African Veterinary Association
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