Direct measurement of pyloric diameter and tone in man and their response to cholecystokinin

Abstract

There is increasing evidence that gastric ulceration is the result of an incompetent pyloric sphincter allowing reflux into the stomach 1 • 2 • Duodenal contents, containing bile and other substances, lower gastric mucosal resistance and the resulting gastritis, more common in the antrum, predisposes to gastric ulceration 3 • 4 • The normal pyloric sphincter not only has some effect on the gastric emptying of liquids and the selection of particulate size of solids, but also prevents duodenogastric reflux. Why does an apparently normal pylorus sometimes allow reflux to occur? To prevent reflux the timing of pyloric closure is important, as any process which upsets this dynamic sequence of events in the antropyloric and duodenal regions causes an alteration in the rate of gastric emptying and/or duodenal reflux s .Local, hormonal or neural factors may affect the motility of this region. Fisher and Cohen 6 have described pyloric dysfunction in gastric ulcer patients when cholecystokinin and secretin failed to increase the pyloric pressure when compared with normal subjects. They suggested that this lack of response could explain why the pyloric sphincter allows reflux. This paper describes a method of direct endoscopic measurement of the pyloric diameter and the assessment of pyloric tone and their response to exogenous cholecystokinin.

A pH-responsive supramolecular polymer gel as an enteric elastomer for use in gastric devices

“…The maximal diameter of a device enabling gastric retention by preventing passage through the pylorus has been previously established as a key parameter. 40 - 42 Considering that the aperture diameter of the resting human pylorus is 12.8 ± 7.0 mm, 14 we prepared a gastric retentive device in a ring-shaped PDMS mold with outer diameter of 32 mm, inner diameter of 28 mm, width of 2 mm, and depth of 2 mm. EE was cut into cuboid sections with the dimensions 6 mm × 4 mm × 2 mm, fitted in the molds and then dried by vacuum.…”

“…Interest in the development of gastric-resident and gastric-retentive devices has been increasing due to their broad applications including: bariatric interventions for nutritional modulation to address the global obesity epidemic, 1 - 3 ingestible electronics for real time physiological monitoring and improving patient health, 4 - 7 and daily dosage forms for prolonged oral drug deliveries. 8 - 12 To achieve prolonged retention in the gastric cavity without exiting through the pylorus (diameter ~ 1.3 cm), 13 , 14 gastric devices are often designed to expand to greater than 2 cm in diameter. At the same time, to ensure the safe delivery of large objects through the narrow esophagus (diameter 1.5-2 cm), 15 those gastric devices are often made of, at least in part, elastic polymers for compacting or folding whole devices into smaller configurations.…”

Case studies in swelling polymeric gastric retentive tablets

“…The lag time for solid emptying is due to the time that is necessary for the stomach to triturate the food into small enough particles (1 -5 mm in diameter). The pylorus has a fasting resting diameter of 12.8 ± 7.0 mm [11] and non-disintegrating dosage forms with a diameter of up to 12 mm may be emptied during the postprandial state [12]. However, as the diameter increases the probability of the tablet emptying during the fed state decreases [13].…”

Direct Effects of Cholecystokinin on Human Gastric Motility

“…These receptors were found to be directly localized on the pyloric muscle of the rat. A direct role of the pyloric sphincter in the inhibition of gastric emptying produced by CCK has also been discussed [14,20], The fact that the CCK activities mea sured in human plasma (10-12-10_n mol/1 [23]) are clearly lower than the threshold concentration for direct CCK effects on smooth muscle (10-9 mol/1) does not exclude the possibility of these direct effects being involved in the normal control processes. CCK is a peptide which is also present in the gastrointestinal nervous system, where it is probably released leading to higher local concentrations [6].…”

“…Moreover, the mechanism of this effect is complex [5,9,17], An inhibition of the spon taneous activity of the fundus and antrum and an interruption of the interdigestive cy cles have also been described [9,17]. In addi tion, various study groups have recently found a pyloric contraction subsequent to CCK application [3,14].…”