[Effect of synthetic motilin on gastric motor activity in conscious dogs].
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The effect of motility on blood flow varies with the nature of the motility and the initiating stimulus, and the mechanical compressing effect on contractions can be modified by intricate local regulatory mechanisms. Although rhythmic contractions usually decrease instantaneous arterial inflow and increase instantaneous venous outflow, mean blood flow may increase, decrease, or remain unchanged. A decrease in mean flow may indicate the predominance of the mechanical effects whereas an increase may be due to an active muscular hyperemia. Both tonic contractions and gut distention decrease total wall blood flow if mechanical compression overrides compensatory mechanisms; the effect is more pronounced on mucosal than on muscularis flow. Oxygen consumption and the capillary filtration coefficient may increase, decrease, or remain unchanged, depending on the degree of distention. The effects of chemicals depend on the interplay and predominance of their vascular, metabolic, and motility actions. When drawing conclusions regarding the effect of motility on blood flow, one must consider the role of local neural and chemical factors, alterations in the metabolic activity of different layers of the gut wall, collateral blood flow, and the mechanical effects of contractions and increased lumen pressure. Increased blood flow has little effect on motility, but severe or total ischemia and hypoxia produce a transient rise in motility followed by a prolonged paralysis.
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Rats were exposed to 7-day hypokinesia and the effect of an enkephalin analog on the secretion of pepsin, amylase, the shape of the glycemic curve and the secretion of gastrointestinal hormones, gastrin and insulin, was investigated. The hypokinetic exposure increased pepsin in the gastric mucosa and amylase in the pancreas, and decreased glycemia and insulin secretion. The analog normalized exo- and endocrine function of the pancreas and the shape of the glycemic curve.
Gastrointestinal hormones containing the C-terminal tetrapeptide of gastrin are involved in calcium homeostasis. The aim of this study was to investigate: 1) the effect of a standard meal (schedule a) and of a duodenal infusion of 5% aminoacid solution (schedule b) on calcium, CT and PTH serum levels in man; 2) the behaviour of these parameters during I.V. infusions of pentagastrin (mcg 1.5/Kg-hour), sincalide (mcg 0.04/Kg-hour) and caerulein (ng 75/Kg-hour) (schedule c). In order to avoid any possible interference by endogenous secretin release, schedule c was performed in 5 patients previously submitted to total gastrectomy. Schedule a and b were studied in 5 healthy volunteers. After a standard meal a slight increase of CT and PTH was measured. Duodenal infusion of aminoacid was followed by hypocalcaemia and slight but constant rise of CT levels, without significant variations of circulating PTH. Pentagastrin, sincalide and caerulein induced a slight but significant hypocalcaemia and a rise of serum CT levels, together with a significant increase of serum PTH. These findings suggest that peptides containing the C-terminal tetrapeptide of gastrin directly affect calcium homeostasis in the absence of secretin release.
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The objectives of this study were threefold. First, we investigated the effects of acute stressful stimuli on gastroduodenal feeding activity after a physiologic meal. Second, we explored the possible role of humoral mediators of these effects by measuring concurrently plasma levels of beta-endorphin, catecholamines, and several gut peptides. Third, we wished to determine whether or not the gut responded selectively to different types of central stimuli. Thus, in 12 healthy volunteers we studied the effects of vertigo and cold pain on the gastrointestinal motor response to a solid meal. Pressure activity was recorded by a low-compliance perfusion system. Plasma concentrations of beta-endorphin and gut peptides were measured by radioimmunoassay, whereas catecholamine levels were measured by high-pressure liquid chromatography. Blood pressure, pulse rate, and skin conductance were also monitored. Labyrinthine vertigo (by otic stimulation with 10 degrees C water; control, 37 degrees C water) and cold pain (immersing hand in 4 degrees C water; control, 37 degrees C water) were simultaneously induced after the meal in each subject according to a 2 X 2 factorial experimental design. Cold pain and labyrinthine stimulation alone or in combination significantly reduced the antral phasic pressure response to solids while elevating plasma levels of beta-endorphin and norepinephrine. These effects occurred within the first 20 min poststimulus and were associated with changes in blood pressure, pulse rate, and skin conductance. Further, in 2 of 6 individuals in whom vertigo was induced by labyrinthine stimulation, a phase 3-like burst of motor activity appeared in the duodenum and migrated aborally. We conclude that centrally acting external stimuli may severely disrupt antral feeding activity. Furthermore, concurrent elevations in plasma levels of beta-endorphin and norepinephrine raise the possibility that these substances may be involved as mediators of the central effects on the gut.
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