The effects of transmural electric stimulation, raising of intraluminal pressure, and application of some drugs on motility and intracellular potentials were studied in isolated chicken bile duct.
1. Peristaltic conduction velocity increased with increasing intraluminal pressure although the range in velocities recorded also increased.
2. Orthodromic and antidromic peristalses were induced by transmural electric stimulation of the hepatic and duodenal sides respectively. Localized contraction was induced by a single square pulse (0.2-1000 msec), but after treatment with tetrodotoxin, stimulation with a pulse below 0.5 msec in duration required a higher voltage to induce an equivalent contraction.
3. The membrane potential was -58.4±1.4 mV. When the bile duct contracted spontaneously, the membrane potential depolarized very slowly and a slow potential occured on which spike potentials of 30-40 mV were superimposed. Over shoot of the spike potential was sometimes observed. The same pattern of electrical activitywas obtained in the pacemaker area also.
4. Adrenaline prodcued a slightly hyperpolarization followed by depolarization. Isoprenaline resulted in hyperpolarization. After the application of atropine, the slow potential induced by transmural stimulation decreased in amplitude and duration and after-hyperpolarization occurred.

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The initiation and the propagation of the ureteral peristalsis were studied through the visual observation and the simultaneous recording of action potentials at both renal pevlis and ureter. The results were summarized as follows:
1) The contraction waves were seen to arise at the proximal end of the renal pelvis. Each wave moved from its origin across the adj acent part of the renal pelvis toward the pelviureteric junction forming a crescentric wave front centering the pelviureteric junction. But some waves failed to propagate not only at the pelviureteric junction but also within the renal pelvis.
2) By electromyographic study, pacemaker potentials were recorded clearly at the proximal end of the pelvis and the interval of the discharge was constant throughout the recording period. Some of the electrical waves failed to conduct within the renal pelvis as well as at the pelviureteric junction.

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In order to elucidate the pathogenesis of achalasia, adult mongrel dogs were used for experimental research on the blood flow to the esophagus following bilateral cervical vagotomy. The control group consisted of forty dogs which were subjected to acute experiment . Thirty dogs were sacrificed forinduced-achalasia-like animal. However only seven of them were eligible for this study.
The measurement of the blood flow was taken from two sites of the esophagus by using the thermoelectrical method, the upper one was located at 2 cm distal to V. hemiazygos, the lower one 2 cm proximal to the esophageal hiatus of the diaphragm.
The following conclusions were obtained.
1. On adrenaline loading, an increasing blood flow to the esophagus was observed in the control group.
2. A decreasing blood flow was demonstrated in the achalasia-like group.
3. The disagreement of the above two measurements could be abolished on administration of an alpha blocking agent; phentolamine.
Accordingly, a decreasing blood flow to the esophagus on adrenaline loading in achalasia-like group in contrast to the control one greatly suggested that the abnormality of the blood flow to the esophagus might predispose to thepathogenesi of the achalasia.

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The role of the antral gastric vagi and the pyloric sphincter on the residual stomach following proximal gastrectomy were studied electromyographically, using adult mongrel dogs. At the first stage of surgery, proximal gastrectomy was performed preserving the bilateral antral gastric vagi followed by esophagogastrostomy by end-to-side anastomosis. The residual stomach was equipped with four bipolar silber needle electrodes and two waterproof strain guages on the wall of the stomach.
At the second and thrid stage of surgery, the same dog subsequently underwent trancal vagotomy and pyloromyotomy at 4 weeks intervals.
Following proximal vagotomy, the interval of the BER in fasting was prolonged. Dysrhythmia was observed quite frequently, and the amplitude and rhythmicity of contractile activities of the residual stomach became lowered and distorted, however, after feeding the interval of the EBR was shortened and dysrhythmia was altered to a regular rhythmic pattern.
Frequent episodes of vomiting were observed following over feeding.
Subsequent trancal vagotomy showed increased incidence of dysrhythmia in fasting, and gave no favourable effects on the vomiting episodes or the amount of feeding. After pyloromyotomy, the amount of feeding could be increased by about 50% from the original optimal amount.

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To clarify the gastric motor function after selective proximal vagotomy (SPV) by electromygoraphy in dogs, I designed the following experimental groups; Group I is the control, untreated dogs; Group II is SPV operated dogs; Group III is selective antral vagotomy (SAV) operated dogs.
The gastric electromygoram was taken from fasted food stimulated, and insulin stimulated dogs in each groups, and the recording was begun two weeks after theoperation.
The results are summarized as follows.
1) The were no significant differences in discharge intervals before and after food and insulin stimulation in all groups.
2) The propagation velocity was delayed markedly in SPV- and SAV-operated dogs compared to the untreated dogs before stimulation.
3) It seemed to be that the delay of propagation velocity at fasting, was more prominent in SAV than in SPV.
Therefore, it is suggested that antral branch might play an important role on the gastric motor function.

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The effects of the synthetic motilin on the gastric motility were investigated in the dogs with innervated antral pouches in fasting state.
The results were as follows:
1) The synthetic motilin stimulated markedly the gastric motor activity in both the contraction pressure and the frequency of the peristalsis.
2) Tetragastrin produced more regular and higher frequent contractions compared with synthetic motilin, but acted to weaker the contraction pressure.
3) In simultaneous administration of the synthetic motilin and the tetragastrin, the synthetic motilin acted more strongly in the contraction pressure, on the other hand tetragastrin in the frequency of the peristalsis.
4) The peristaltic contractions induced by synthetic motilin were completely abolished by the administration of the atropine sulfate.
5) Under medical vagotomy, synthetic motilin was not able to produce any peristatlic contractions, but tetragastrin stimulated strongly the gastric motility.

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