Kazumoto Fujii

THE CENTRAL NEURAL MECHANISM OF THE GASTRIC MOTILITY IN THE DOG'S MEDULLA OBLONGATA ON THE VAGAL INHIBITORY AND EXCITATORY REFLEXES

The influences of the vagal inhibitory and excitatory reflexes on the gastric motor centers in the dogs 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.

INFLUENCE OF CIMETIDINE ON NEURO-HUMORAL EXCITATORY RESPONSES OF GASTRIC SECRETION AND MOTILITY IN DOG

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.

EFFECTS OF PHYSOSTIGMINE AND DUVADILAN ON AN ATROPINE-RESISTANT CONTRACTION OF DOG'S STOMACH

Effects of atropine, physostigmine, duvadilan and tetrodotoxin on the mechanical activity of the longitudinal muscle preparation of dogs 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.

AN ATROPINE-RESISTANT CONTRACTION OF DOG'S STOMACH IN RESPONSE TO STIMULATION OF THE VAGUS AND SPLANCHNIC NERVES

1. A study was made in vivo experiments of a contraction of stomach of the dog to stimulation of the extrinsic nerves, medulla oblongata and thoracic cord in the presence of atropine. 2. An atropine-resistant contraction of stomach was produced without accompanying any preceding relaxation of stomach motility. It seems to deny that an atropine-resistant contraction appears to be a rebound phenomenon. 3. An atropine-resistant contraction was produced in prolonged stimulation. A delay of latency to produce a contraction of stomach was more than 27 sec and a contraction was decreased in amplitude and frequency in the presence of atropine.