To clarify the mechanism of delayed gastric emptying after vagotomy and the related problem whether the vagotomized stomach develops pylorospasm under any condition, the author studied the motor function of the canine stomach with the use of electromyography when warm water was instilled before and after vagotomy.
Regardless of whether vagotomy had been performed or not, a marked excita-tion of the pyloric portion of the stomach occurred, resulting in a spasm-like abnormal excitation and anti-peristalsis as the intragastric pressure was elevated by instillation of water. However, the vagotomized stomach required much more water than the non-vagotomized one to develop the same degree of excitation of the pyloric portion. This difference was probably due to hypomotility or hypotonicity of the vagotomized stomach. On the other hand, vagotomy did not cause pylorospasm or abnormal excitation of the pyloric portion, although hypomotility of the stomach was present.
The above results suggested that the vagotomized stomach developed hypo-motility or hypotonicity first, which led to stasis and retention of the gastric content. Furthermore, the elevation of intra-gastric pressure due to this stasis and retention was followed by spasm-like abnormal excitation of the pyloric portion and anti-peristalsis. Therefore, 'pylorospasm' was considered to occur secondarily as a result of gastric stasis and retention, but not primarily by vagotomy.
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