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Abstract
The digestive tract is highly autonomous and the extrinsic nerves serve largely to
prevent response to every stimulus. After vagotomy or splanchnicotomy peristalsis
is often so active that the animal dies of inanition.
Normal aborad peristalsis appears to follow gradients of rhythmicity, irritability,
latent period, metabolism, and muscular strength, running from duodenum to terminal
ileum. These gradients might theoretically be reversed either by raising the irritability
of the lower end of the gut or by depressing that of the upper end.
It may perhaps be stated as a law that irritation at any point in the bowel tends
to slow the progress of material coming from the stomach toward it, and to hasten
the progress of material moving caudad away from it. If the irritation is severe enough
the result is an emptying of the digestive tract both ways from the lesion, with vomiting
and diarrhea.
When, in rabbits, enough turpentine was injected into the tissues about the ileocecal
sphincter to produce considerable injury, the animals suffered from diarrhea and the
colon was emptied. The ileum was emptied orad and food residues were held back in
the duodenum. Peristaltic rushes were few; they were hard to start, and they were
slowed and stopped in the lower bowel.
The whole bowel was unusually sensitive to faradic stimuli, and in most of the experiments
the normal gradient in irritability from duodenum to ileum was reversed. With the
increased irritability of the bowel the latent periods were shortened, and the fact
that this change was more marked in the lower ileum than in the duodenum caused the
normal gradient (in latent period) to be flattened.
Segments of gut excised from the injured animals and placed in warm aerated Locke's
solution behaved normally, showing that the failure of the bowel to pass onward its
contents was not due to injury to the muscle.
Chemical injury to the ileocecal region in animals with vagi and splanchnics cut and
much of the conducting system in the bowel degenerated still produced backpressure
in the small bowel and marked slowing of rush waves. This suggests that the flattening
of gradients had something to do with the failure of conduction.
The work suggests that in treating dynamic ileus attempts should be made first, to
remove nervous inhibition, perhaps by splanchnic blocking or by spinal anesthesia,
and second, to restore the normal dynamic gradient by giving food, and by avoiding
morphine and irritation to the lower bowel. The various methods of inducing peristalsis
postoperatively are briefly reviewed.
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Article info
Publication history
Received:
February 18,
1929
Identification
Copyright
© 1929 Published by Elsevier Inc.
