scholarly journals Effect of Prostacyclin on Gastric Emptying and Secretion in Rhesus Monkeys

1980 ◽  
Vol 78 (6) ◽  
pp. 1476-1479 ◽  
Author(s):  
P. Terez Shea-Donohue ◽  
L. Myers ◽  
D.O. Castell ◽  
A. Dubois
1983 ◽  
Vol 245 (2) ◽  
pp. G196-G200
Author(s):  
P. T. Shea-Donohue ◽  
N. Adams ◽  
J. Arnold ◽  
A. Dubois

Recent studies have demonstrated the presence of enkephalins in gastric neurons and endocrine cells; however, their role in the regulation of gastric function is unknown. The effect of Met-enkephalin (MET), the stable analogue of Met-enkephalin [D-Ala2]Met-enkephalinamide (DMET), and the opiate receptor antagonist naloxone were studied in five chair-adapted rhesus monkeys. A dye-dilution technique was used to determine simultaneously fractional emptying rate, hydrogen, sodium, potassium, and chloride ion output, and fluid output. Both MET and DMET significantly inhibited fractional emptying rate and H+ secretion following an 80-ml water meal. Only MET, however, significantly altered fluid and sodium ion output. Naloxone had no effect on gastric function following the water meal.


1982 ◽  
Vol 243 (3) ◽  
pp. G200-G203
Author(s):  
J. N. Hunt ◽  
P. R. McHugh

Disodium edetate (EDTA, 1 g/l) in test meals of water slowed gastric emptying strongly in one human and in four rhesus monkeys. When the binding sites of the EDTA were loaded with calcium before it was given in the test meal, there was little effect on gastric emptying. It is suggested that EDTA takes up calcium from the “tight junctions” of the duodenal epithelium. As a result a signal is set up that slows gastric emptying. It is postulated that the anions of fatty acids produced during the digestion of triglycerides in the duodenum also slow gastric emptying by the same mechanism. We explain how fats, carbohydrates, and proteins could all slow gastric emptying by operating on the same receptor.


1994 ◽  
Vol 64 ◽  
pp. 283
Author(s):  
Kenji Yogo ◽  
Ken-ichi Ozaki ◽  
Hisanori Takanashi ◽  
Masao Kotoh ◽  
Michitaka Akima ◽  
...  

1993 ◽  
Vol 265 (2) ◽  
pp. R371-R375 ◽  
Author(s):  
T. H. Moran ◽  
P. J. Ameglio ◽  
G. J. Schwartz ◽  
H. J. Peyton ◽  
P. R. McHugh

A role for the brain/gut peptide cholecystokinin (CCK) in the control of gastric emptying has been proposed. In the present studies, we have used a potent type A CCK-receptor antagonist (devazepide) to examine the quantitative contribution of endogenously released CCK in the control of liquid gastric emptying of 100 ml lipid, protein, and carbohydrate test loads in rhesus monkeys. Emptying was studied in conscious monkeys equipped with chronic indwelling gastric cannulas. Prior intragastric administration of devazepide (1.0-320 micrograms/kg) differentially affected the 10-min emptying of glucose (0.125/ml), peptone (4.5%), and Intralipid (4.5%). Glucose emptying was not affected by any dose of the CCK antagonist. The emptying of peptone was accelerated by doses of 10 micrograms/kg or higher. This effect, however, was only partial and plateaued at a dose of 100 micrograms/kg. The gastric emptying of Intralipid was accelerated at a dose of 32 micrograms/kg, and the inhibitory effect of the Intralipid was completely eliminated at a dose of 320 micrograms/kg. At this dose of devazepide, the Intralipid test meal emptied from the stomach at the same rate as physiological saline. These data demonstrate that in rhesus monkeys endogenously released CCK 1) does not play a role in the control of glucose emptying, 2) is a partial mediator of the inhibitory action of peptone on gastric emptying, and 3) is the primary inhibitory mediator in the control of the gastric emptying of Intralipid.


1988 ◽  
Vol 255 (6) ◽  
pp. G767-G771
Author(s):  
A. Dubois ◽  
D. Nompleggi ◽  
D. O. Castell

We studied the effect of the specific H2 receptor agonist dimaprit on gastric emptying using a dye dilution technique in five chair-adapted rhesus monkeys to determine simultaneously gastric emptying and H+ secretion. Continuous subcutaneous injections of either saline alone or dimaprit (15, 30, 60, 120, and 240 nmol.kg-1.min-1) were given in random order on separate days. Both fractional emptying rate and H+ output were significantly increased by higher doses of dimaprit, with resulting twofold concurrent increase of intragastric H+ concentration. Because intragastric administration of H+ decreases gastric emptying and secretion, we evaluated the possibility that the stimulatory action of a histamine H2 agonist was underestimated when gastric pH was greater during control than after dimaprit. When exogenous HCl was added to the stomach to achieve H+ concentrations similar to those measured after dimaprit, both fractional emptying and H+ secretion were decreased twofold. When these "acidified control values" were used as a point of comparison, the stimulatory effect of dimaprit on both fractional emptying and gastric secretion was greater, suggesting that the stimulatory actions of dimaprit are underestimated if one does not take into account the differences in intragastric H+ concentrations.


1986 ◽  
Vol 250 (5) ◽  
pp. R764-R769 ◽  
Author(s):  
P. H. Robinson ◽  
T. H. Moran ◽  
P. R. McHugh

To assess the mechanism by which the anorectic agent fenfluramine influences feeding, we examined in Macaca mulatta the effect of intragastric fenfluramine (2 mg/kg) on both feeding and the gastric emptying of saline and glucose test meals. Gastric emptying was measured by the dye-dilution technique, using chronic indwelling intragastric cannulas. The emptying of normal saline was inhibited by fenfluramine as was the initial bolus phase of the emptying of glucose. In contrast, the subsequent controlled phase of glucose emptying was unaffected in two out of four animals, slightly inhibited in one, and strongly inhibited in only one monkey. Rhesus monkeys trained to drink a glucose solution to satiety drank, on average, 21% less after fenfluramine. The emptying of the consumed glucose solution from the stomach was reduced by 39%, whereas gastric volume at satiety was reduced by only 10%. The reduction of intake was strongly related to the degree of inhibition of gastric emptying. These results support an important role for the inhibition of gastric emptying in fenfluramine-induced suppression of feeding.


2007 ◽  
Vol 53 (4) ◽  
pp. 912-918 ◽  
Author(s):  
Kenji Yogo ◽  
Mitsu Onoma ◽  
Ken-ichi Ozaki ◽  
Masao Koto ◽  
Zen Itoh ◽  
...  

1999 ◽  
Vol 276 (4) ◽  
pp. R997-R1002 ◽  
Author(s):  
Timothy H. Moran ◽  
James B. Wirth ◽  
Gary J. Schwartz ◽  
Paul R. McHugh

We examined the relationships between gastric volume and duodenal glucose load in the regulation of gastric emptying in adult male rhesus monkeys. Intragastric glucose loads (0.125 g/ml) of volumes ranging from 150 to 375 ml empty from the stomach at the same rate from 20 to 120 min. However, to achieve these equivalent emptying rates, progressively larger volumes were emptied in the initial 20 min with increasing gastric volume. Duodenal glucose infusions dose dependently inhibited the 10-min emptying of various volumes of intragastric saline. Although increasing gastric volume resulted in increased emptying, duodenal glucose right-shifted the relationship between initial gastric volume and volume emptied. These data demonstrate that liquid nutrient gastric emptying represents an interaction between gastric volume and nutrient-induced duodenal feedback. For controlled duodenal caloric delivery rates to be established, sufficient nutrient emptying must occur to increase the magnitude of duodenal feedback to withhold a given gastric volume.


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