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In order to identify the mechanisms responsible for the inhibition of gastric secretion observed during acidification of the duodenal bulb, dogs were prepared with a gastric fistula (GF), Heidenhain pouch (HP), and pancreatic fistula. The duodenal bulb (5 cm) was separated from the stomach by a mucosal septum at the pyloric end and was brought to the surface in a mucocutaneous fistula distally. After the first series of experiments were completed, the dogs were reoperated and the duodenal bulb was completely separated from the stomach. The experiments were then repeated. Perfusion of the innervated duodenal bulb with 8 mEq of HC1 per hr resulted in 50% inhibition of pentagastrin (2 μg per kg-hr) -induced acid secretion from the GF and slight stimulation of pancreatic volume, bicarbonate, and protein output. Acid and pepsin secretion from the HP were unchanged by acidification of the bulb. A small dose of synthetic secretin (0.2 U per kg-hr) increased pancreatic secretion more than did bulbar acidification but did not inhibit acid secretion. A larger dose of secretin (1.6 U per kg-hr) caused 50% inhibition of acid secretion from both the GF and HP. Following the surgical separation of the duodenal bulb from the pylorus, acidification of the bulb failed to inhibit gastric secretion from the GF as well as from the HP. We interpret these results as evidence for the existence of a neural reflex, triggered by acid in the duodenal bulb, and inhibiting gastric secretion. Earlier studies by several groups have shown that acidification of the bulb inhibited HP secretion, thus indicating a hormonal mechanism. We cannot explain the failure to find evidence of such a mechanism in this study.

Impulses have been recorded from single vagal gastric motor axons in sheep during reflex gastric contractions. Several different patterns of activity associated with contractions of different parts of the stomach were found. Each unit had a stable and characteristic pattern of discharge. The discharge of a unit could be modified by a general excitatory stimulus e. g., acidification of the gastric contents or by afferent “feed-back” from the part of the stomach that was contracting.

In acute experiments on chloralosed cats gastric motility was recorded with a rubber balloon system kept at constant intragastric pressure under experimental conditions not requiring abdominal surgery.-Electric stimulation of the central end of either a small vagal branch at the level of the diaphragm or of one vagal nerve at the level of the neck, while the opposite vagal nerve was left intact produced profound reflex relaxation of the stomach. Also the efferent pathway of the relaxatory reflex was in the vagal nerves.-The reflex relaxation persisted after administration of atropine, which shows that it was not due to reflex suppression of prevailing activity of the vagal cholinergic motor fibres. It was also independent of adrenergic mechanisms, since it persisted after administration of guanethidine in doses known effectively to block the adrenergic intestino-gastric inhibitory reflex. This vago-vagal relaxatory reflex response thus showed the same characteristics as the gastric response elicited by efferent stimulation of the high-threshold vagal relaxatory fibres.-It is concluded that this vago-vagal reflex originates, at least partly, from abdominal structures, with the efferent pathway consisting of the relaxatory, high-threshold fibres producing pronounced gastric relaxation. This vago-vagal relaxatory reflex may be involved in receptive relaxation of the stomach.

Adequate electrical stimulation of the central cut end of the abdominal vagus invariably raises the blood pressure 30 mm Hg due to visceral and somatic vasoconstriction without change of heart rate. This response is accompanied by a reflex gastric relaxation which persists at reduced amplitude after abdominal vagotomy, an increase of respiratory amplitude without change of rate, and by inhibition of the knee-jerk reflex. The receptors for the pressor reflex respond to distension of the esophagus, cardia, stomach or pylorus, while those for the gastric reflex respond to distension of the pylorus and to changes of pH in the duodenum.

In studying the nerve pathways involved in the reflex inhibition of hunger contractions by distention of a Thiry fistula loop in the dog,1 it was noticed that a previous long-continued distention of the loop brought about a lower threshold for the reflex.In the experiments here reported, five animals were prepared with Thiry fistulae in the usual manner, the loops being 15-20 cm. long and taken from the upper ileum. After complete recovery the dogs were trained to swallow a stomach tube and to lie quietly on the table without any restraint. Gastric movements were recorded by the customary balloon-tambour method. The intestinal loops were distended by air inflation of a thin-walled balloon which was over-size relative to the lumen of the gut. The balloon was tied over a glass rod so that the expansion would be entirely lateral and the pressure readings would closely approximate the pressure actually applied to the intestinal wall. All records were made after a fasting period of 18-24 hours. In testing for ...

SummaryAcid in upper small intestine causes immediate inhibition of gastric motility. Sixteen dogs were prepared with gastric fistula and/or Heidenhain pouch plus a Maydl fistula of upper jejunum. ...

The effect of distension of a small or large intestinal loop on the ileo-cecal sphincter (ICS) in the cat was studied with a flow-recording technique. Distension of a small or large intestinal loop, isolated from the adjacent intestine, but with its mesenteric vascular and nervous supply intact, elicited a contraction of the ICS concomitant with an inhibition of the adjacent large and small intestinal motility. Vagal and pelvic nerve section did not affect the response to distension of the ICS nor exclusion of the adrenal glands from the circulation. The sphincter reflex could be entirely or almost entirely eliminated by cutting both the splanchnic and lumbar colonic nerves, but not one or the other. Spinal anesthesia bocked the reflex response indicating a spinal reflex arc. The reflex persisted after atropine and propranolol, while both guanethidine and phenoxybenzamine completely abolished the reflex contraction of the sphincter. The present results indicate that the excitatory intestino-ileo-cecal sphincteric reflex is a spinal reflex with the main afferent and/or efferent fibres located within the major splanchnic and lumbar colonic nerves. The excitatory motor response in the sphincter is adrenergic and mediated via alpha-receptors.

The reflex effects of distension and contraction of the gastric antrum on corpus-fundus motility were studied in anesthetized cats. Besides a vagally mediated reflex corpus-fundus relaxation, antral distension elicited a prompt reflex inhibition of corpus-fundus contractions that was present also after vagotomy. In vagotomized animals this inhibitory reflex persisted also after cervical spinal cord transection, but was abolished by spinal anrsthesia or by guanethidine. Stepwise increases of antral distension revealed that the reflex corpus-fundus inhibition appeared already at distending pressures of 5–10 cm H2O, then increased in a graded fashion and could be maintained for at least 10 min if a steady distension was applied. Also “isometric” antral contractions were effective in eliciting the reflex corpus-fundus inhibition. — It is concluded that activation of slowly adapting “tension receptors” in the antral gastric wall inhibits gastric (corpus-fundus) motility via a spinal reflex mechanism, mediated by splanchnic adrenergic fibres that seem to suppress the intramural excitatory cholinergic neurons. This gastro-gastric adrenergic inhibitory reflex seems to be activated concomitantly with a vago-vagal gastro-gastric relaxatory reflex. It is suggested that these two suppressive reflex mechanisms play an important role in regulation of gastric motor functions.

Publisher Summary This chapter focuses on ion transport in gastric mucosa. The muscosal surface of the stomach has a large number of openings, which are the gastric pits that produce the gastric secretion. The physiology of secretion can be roughly divided into two parts: one concerned with the basic mechanism by which the cells elaborate the secretion and the second with the control mechanisms. Gastric secretion is controlled by both hormonal and reflex mechanisms. The taste or smell of food can cause the stomach to secrete under conditions where the food does not come in contact with the mucosa. Food in contact with the stomach stimulates the liberation of the hormone gastrin from the antrum into the blood stream. The gastrin in the blood reaches the stomach and stimulates the formation of gastric juice. When the pH of the stomach contents reaches about 2, further liberation of gastrin is inhibited, the acid acting as a negative feedback to gastrin secretion. The chapter discusses the anatomy and physiology of the stomach. Active transport of H+ and Cl− is also analyzed in the chapter.

The effect of intravenous infusion of gastrin II on gastric and colonic motor activity was studied in 12 patients; gastric acid output was also measured. Administration of gastrin at near-maximal dose levels stimulates the motor activity of the antrum but has no measurable effect on the activity of the proximal colon, sigmoid, or rectum. The results suggest that gastrin plays a part in the regulation of gastric motility but that it is not a mediator of the gastro-colic reflex.

Numerous investigators have reported a delay in gastric evacuation as a result of placing acid, fat, gastric juice, etc., in the duodenum or other parts of the small intestine. The effect has generally been attributed to a reflex (the “Hirsch v. Mering reflex”) causing tonic contraction of the pyloric sphincter. However, two studies record inhibition of contractions of the pars pylorica following the introduction of acid1 or fat2 into the duodenum. Apparently both investigations were made upon the empty stomach, though Edelmann2 observed inhibition of gastric contractions during secretion of gastric juice. There are no data in either report to prove that the phenomenon occurs in the full stomach or has any bearing on the mechanism of gastric evacuation.We studied the effect of placing various substances in the duodenum while recording graphically the tone changes in the pyloric sphincter by means of the pressure tonometer,3 and the contractions of the pars pylorica by means of a balloon placed in the pylo...

The walls of the normal fasting stomach are maintained in coaptation by a state of tonus of its muscular coats, with recurrent periods of superimposed peristaltic activity. With the first taste of food there follows an immediate relaxation of gastric tonus with usually a fairly complete inhibition of peristalsis, resulting in a widening of the gastric lumen to accommodate the expected food injesta. This is the normal gastric feeding reflex (fig. 1). In the presence of various types of extragastric pathologic change, usually intra-abdominal or pelvic, this normal feeding reflex is distorted. Instead of relaxation there is an immediate increase in tone, with or without superimposed peristalsis. The degree of distortion roughly parallels the intensity of the sensory or psychic stimuli (fig. 2 A and B ) and is not influenced by the degree of acidity of the gastric secretions (table 1). These distortions of the normal gastric feeding reflex are