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Effects of atropine, physostigmine, duvadilan and tetrodotoxin on the mechanical activity of the longitudinal muscle preparation of dog's stomach in vitro experiments and on the motility of stomach in the same animal in vivo experiments were investigated. 1. The latency of an atropine-resistant contraction which was produced by stimulation of vagus nerve was increased in period in accordance with the augmentation of concentration of atropine in vitro experiments. 2. Physostigmine reconstructed the atropine-resistant contraction which was abolished by duvadilan as well as the cholinergic contraction which was abolished by atropine in vivo experiments. 3. Duvadilan abolished the cholinergic and atropine-resistant contractions in vitro, but in vivo experiments duvadilan abolished only the atropine-resistant contraction. 4. An atropine-resistant contraction was completely abolished by administration of tetrodotoxin. But the direct electrical stimulation of the muscle caused the contraction of it which was blocked by tetrodotoxin.

The influences of the vagal inhibitory and excitatory reflexes on the gastric motor centers in the dog's medulla oblongata were investigated. Dogs were anaesthetized with Nembutal, and supplemented Gallamine at need. The brain stem was transected on the level of inferior colliculi of midbrain, the spinal cord transected on the level of between C1 and C2. Bilateral splanchnic nerves were also severed. Electrical activities from the inhibitory and excitatory areas in medulla oblongata were recorded by using a concentric circle electrode which was inserted into medulla oblongata from the dorsal surface of it. Following results were obtaind. 1) Electrical activities of the gastric inhibitory areas were classifed into three types (see Table 1). Type I: The augmentation of electrical activities of the gastric inhibitory areas during theinhibitory reflex were associated with the diminution of them during the exictatory reflex. Type II: Although electrical activities of the gastric inhibitory areas were augmented during the inhibitory reflex, any changes of them were not obtained during the excitatory reflex. Type III: Any changes of electrical activities of the gastric inhibitory areas were not obtained during both inhibitory and excitatory reflexes. 2) Electrical activities of the gastric excitatory areas were classified into two types (see Table 2). Type I: The diminution of electrical activites of the gastric excitatory areas during the inhibitory reflex were associated with the augmentation of them during the excitatory reflex. Type II: Although any changes of electrical activities of the gastric excitatory areas were not observed during the inhibitory reflex, they were augmented during the excitatory reflex.

The influence of electrical stimulation of central cut end of the glossopharyngeal nerve on the vagal inhibitory and excitatory reflexes of gastric movements were investigated. Frogs and bullfrogs were employed in all experiments under urethan anaesthesia and also immobilized with 1% solution of d-tubocurarine chloride. Bilateral splanchnic nerves were previously severd, and so the stomach was innervated through the vagus nerves only. 1. The vago-vagal inhibitory reflex of gastric movements was depressed or abolished during the maintenance of stimulation of the glossopharyngeal nerve. But, the vago-vagal excitatory reflex of gastric movements was augmented in the one example and in the other example it was depressed during the glossopharyngeal stimulation. 2. The labyrintho-vagal excitatory reflex of gastric movements was excited during the maintenance of stimulation of the glossopharyngeal nerve.

The influence of intravenous administration of cimetidine on excitatory response of gastric secretion and motility of innervated or denervated pouches caused by electrical stimulation of vagal and splanchnic nerves and administration of tetragastrin or histamine respectively were investigated. Dogs were anesthetized with nembutal, and also immobilized with gallamine tricthiodide. The following results were obtained. (1) Administration of cimetidine inhibited the augmentation of gastric juice and acid output from the innervated corpus pouch by vagal and splanchnic nerve stimulation and vestibulo-gastric excitatory reflexes of gastric secretory functions via the vagal or splanchnic nerve. (2) Augmentation of gastric acid output from the denervated corpus pouch caused by electrical stimulation of vagal and splanchnic nerves was inhibited by administration of cimetidine. (3) Administration of cimetidine inhibited the augmentation of acid output from denervated corpus pouch caused by injection of tetragastrin or histamine. (4) The excitatory responses of gastric motility caused by nerve stimulation and administration of tetragastrin or histamine could not be effected by cimetidine. (5) No changes were observed in the gastric venous blood flow by continuous intravenous injection of cimetidine, but by rapid injection both the flow was augmented and the systemic blood pressure decreased transiently. These results indicate that histamine stimulates gastric secretory cells directly.

The effects of tonic and rhythmic contraction of the intestine on the arterial and venous blood flow through the intestinal segment were investigated in dogs.Intestinal contractions always caused periodicity in the arterial and venous blood flow. The correlation between intestinal contraction and the arterial and venous flow was classified into three patterns; the contraction phase type, relaxation phase type and combination type were observed in tonic contraction, and the contraction phase type and relaxation phase type in rhythmic contraction.In the contraction phase type, augmentation of venous flow and diminution of arterial flow was elicited during the contraction period. In the relaxation phase type, diminution of venous and arterial flow during the contraction period was followed by sustained augmentation of flow during the relaxation period. The combination of these two patterns is the combination type.Augmentation of venous outflow during the contraction period was produced by expelling blood from the intestinal wall, as the arterial inflow was diminished during this period. Augmentation of arterial and venous flow during the relaxation period was caused by vasodilatation due to prolonged compression of the blood vessel by contraction of the intestinal musculature.

The influence of electrical stimulation of the medulla oblongata and associated structure on gastric motility of anesthetized and non-anesthetized dogs was studied.Increase in gastric motility was observed on stimulation of the dorsal nucleus of the vagus, the solitary tract and its nucleus and the dorsal region of the reticular formation.Inhibition of gastric motility was obtained on stimulation of the solitary tract and its nucleus, the dorsal region of the reticular formation and the dorsal nucleus of the vagus.The efferent pathways for excitatory effects from the medulla oblongata were not only the vagus nerves but also the splanchnic nerves. The efferent pathways for inhibitory effect were also the splanchnic nerves and the vagus. Diagram presented in FIG.7 illustrates the regulation center upon the excitatory and inhibitory centers for stomach motility and the efferent pathways from them to the stomach.

In order to clarify the role of histamine in the neuro-humoral excitatory mechanism in the stomach, the effect of cepharanthine (an inhibitory agent of histamine release from mast cells) on excitatory response of gastric movement and increase in gastric mucosal histamine content caused by nerve stimulation (vagus and splanchnic nerves) or administration of tetragastrin were investigated in dogs. The animals were anesthetized with pentobarbital sodium and immobilized with gallamine triethiodide. The following results wee obtained. Increase of gastric mucosal histamine content caused by vagal and splanchnic nerve stimulation and administration of tetragastrin was inhibited by administration of cepharanthine. Cepharanthine inhibited the tonic contraction of the innervated antral pouch or isolated antral circular muscle strip caused by stimulation of vagus nerve. Tonic contraction of the innervated antral pouch caused by electrical stimulation of the splanchnic nerve after nicotinization of celiac and superior mesenteric ganglia was inhibited by administration of cepharanthine. Cepharanthine inhibited motor excitatory response of the denervated corpus pouch caused by stimulation of vagus and splanchnic nerves and by administration of tetragastrin. These results support the theory that cepharanthine inhibits the release of histamine from histamine-secreting cells in the gastric mucosa. It is suggested that histamine plays an important role in the neuro-humoral excitatory mechanism of gastric movement.

Fujii, K., Okajima, M., Kawahori, K., Murakami, Y. and Shimatani, T. Effect of α2-adrenergic receptor antagonist (Midaglizole) on gastrointestinal motility in conscious dogs. Jpn. J. Smooth Muscle Res., 1989, 25 (4), 000-000, 1989 To clarify the physiological role of the mechanism that adrenergic nerve inhibits Ach release from intramural cholinergic nerve endings, the influence of Midaglizole, α2-adrenergic receptor antagonist, to postpran-dial gastrointestinal motilities in conscious dogs was investigated.Postprandial motilities of gastric antrum, duodenum, ileum, and colon were significantly enhanced by Midaglizole (3.0-5.0 mg/kg body weight, i.v, ). These excitatory responses were abolished by atropine (0.05-0.1 mg/kg body weight, i.v.). On the other hand, in most cases (29 cases out of 32), when Midaglizole was administered during quiesent phase of IMC, no change occurred in gastrointestinal motility. However, after subliminal dose of pentagastrin or cisapride, which stimulated Ach release from intramural cholinergic neuron without development of motility, was administered, Midaglizole induced phasic, postpran-dial motility-like contraction in gastrointestinal tract. Even in the fasted state, when Midaglizole was administered intragastrically, irregular contractions with high amplitude occurred in every regions from gastric antrum to colon. And these excitatory responses were abolished by atropine. Similar reaction was observed also in truncal vagotomized dogs.These results suggest that it is the physiological mechanism that adrenergic nerve presynaptically inhibits Ach release from intramural cholinergic neuron, which is the main mechanism of development of postprandial motility, acting on α2-adrenergic receptor, and has tonic control of postprandial motility.

The effects of tonic and rhythmic contraction of the gut on venous blood flow and oxygen saturation in venous blood through an intestinal segment were investigated in anesthetized dogs.Intestinal contraction caused periodicity not only in venous outflow but also in oxygen saturation in venous blood.(1) It was observed in tonic contraction that augmentation of venous outflow synchronized with reduction of oxygen saturation in venous blood and that diminution of venous outflow produced an increase of oxygen saturation in venous blood.(2) In rhythmic contraction, the correlation between venous outflow and oxygen saturation in venous blood could be classified into two patterns. In the first pattern fluctuations of venous outflow corresponded reciprocally to fluctuations of oxygen saturation, and in the second pattern both curves fluctuated parallel to each other.The mechanism of the correlation between venous outflow and oxygen saturation in venous blood in each type is discussed.

The effect of rhythmical contraction of the spleen on the splenic venous flow was studied. The rate of blood flow through the splenic vein was determined in dogs which maintained an almost constant systemic blood pressure before and after the rhythmical contractions was induced. Normal splenic blood flow averaged 2.77ml per minute, but increased to 3.22ml per minute on the average during the period of rhythmical contractions. This increase corresponded to 16.2% of the normal splenic blood flow. This suggests that the rhythmical fluctuation in splenic blood flow accelerates the blood flow in the portal vein.