Captopril inhibits secretin-induced pancreatic bicarbonate output

2001 ◽  
Vol 120 (5) ◽  
pp. A338-A338
Author(s):  
M HOWARDMCNATT ◽  
A FINK
Keyword(s):  
1979 ◽  
Vol 236 (5) ◽  
pp. E539 ◽  
Author(s):  
M S Kim ◽  
K Y Lee ◽  
W Y Chey

In four dogs with a modified Herrara pancreatic fistula and gastric cannula and three dogs with two duodenal cannulas, ingestion of a meat meal resulted in a significant and sustained increase in the mean plasma immunoreactive secretin concentrations, from mean fasting levels of less than 10 pg/ml to 25--55 pg/ml. This increase in the plasma secretin concentration coincided with a marked increase in pancreatic bicarbonate output and frequent decreases in the mean proximal duodenal pH to less than 4.5 from the range of 6.5 in the fasting state. Intravenous administration of cimetidine, 150 mg, produced a marked suppression of postprandial increases in both pancreatic bicarbonate output and plasma secretin concentration. Moreover, the postprandial duodenal pH rarely reached below 5.0 after cimetidine administration. These studies indicate that plasma secretin concentration does increase significantly after a meal. The postprandial increase in plasma secretin concentration appears to depend on the gastric acid delivered in the proximal duodenum. A possible physiological role of secretin in the pancreatic secretion after a meal is indicated by these findings.


1963 ◽  
Vol 204 (2) ◽  
pp. 251-256 ◽  
Author(s):  
J. H. Baron ◽  
C. V. Perrier ◽  
H. D. Janowitz ◽  
D. A. Dreiling

By cannulation of the major pancreatic duct in six dogs with chronic Thomas type duodenal fistulas, dose-response curves have been obtained for the volume and bicarbonate output of pancreatic secretion stimulated by secretin (Vitrum). With single rapid intravenous injections (0.5–15 U/kg) or continuous intravenous infusions (1–16 U/min), increased doses of secretin produced increased volumes of pancreatic juice and bicarbonate outputs up to a maximum. This maximum alkaline output of the pancreas was reached at doses ranging from 7.5– 12.5 U/kg for single injections, and 4–16 U/min for infusions. In each dog supramaximum doses led to a fall in juice volume and bicarbonate output, unaccompanied by side effects. With supramaximum doses or intravenous infusions lasting longer than 30–90 min, bicarbonate concentration fell independently of juice volume. The chloride concentration consistently varied inversely with bicarbonate concentration. The sodium, potassium, and amylase concentrations were unaffected by rate of flow. Repeated measurements of basal secretion showed considerable variation. Coefficients of variation were low for repeated measurements of secretin-stimulated secretion, the most repeatable measurement being the maximum output of pancreatic juice in the first 15 min after a single injection which, in each of the six dogs, was almost identical to the plateau 15 min during infusion.


Gut ◽  
1993 ◽  
Vol 34 (7) ◽  
pp. 872-880 ◽  
Author(s):  
C M Brown ◽  
C F Snowdon ◽  
B Slee ◽  
L N Sandle ◽  
W D Rees
Keyword(s):  

1996 ◽  
Vol 270 (1) ◽  
pp. G113-G122 ◽  
Author(s):  
J. Dalenback ◽  
L. Fandriks ◽  
L. Olbe ◽  
H. Sjovall

Human gastric interdigestive acid and bicarbonate outputs vary cyclically in association with the migrating motor complex (MMC). These phenomena were studied in 26 healthy volunteers by constant-flow gastric perfusion, with continuous recording of pH and Pco2 in mixed gastric effluent and concomitant open-tip manometry of gastroduodenal motility. Stable acid and bicarbonate outputs were registered during less than 50% of the MMC cycle. Acid secretion started to increase 71 +/- 3% into the cycle, with maximum output during antral phase III. Bicarbonate output increased biphasically 1) 40 +/- 5% into the cycle, coinciding with reflux of bile, and 2) at the end of duodenal phase III when the aspirate was devoid of bile. The bicarbonate peak associated with phase III was abolished by atropine (0.01 mg/kg iv, n = 8) and by pyloric occlusion (n = 9) but remained unchanged after omeprazole (n = 10). The acid peak was abolished by both atropine and omeprazole. It is concluded that the MMC-related changes in acid and alkaline outputs represent two different and independent phenomena. Acid secretion cyclicity is due to periodical variations in cholinergic stimulation of the parietal cells. In contrast, the phase III-associated increase in bicarbonate output is due to duodenogastric reflux.


1988 ◽  
Vol 254 (3) ◽  
pp. G436-G443
Author(s):  
W. Niebel ◽  
C. Beglinger ◽  
M. V. Singer

In two sets of dogs with gastric and pancreatic fistulas, we studied the effect of atropine on pancreatic bicarbonate output and release of secretin in response to intraduodenal HCl before and after stepwise removal of the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy alone and truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Ganglionectomy alone did not alter the incremental bicarbonate response to HCl. Truncal vagotomy alone significantly (P less than 0.05) decreased the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high (6 to 24 mmol/h) loads of HCl. Additional ganglionectomy restored the bicarbonate response to prevagotomy levels. With the extrinsic nerves intact and after ganglionectomy, but not after truncal vagotomy and truncal vagotomy plus ganglionectomy, intravenous atropine (14 nmol.kg-1.h-1) significantly reduced the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high loads of HCl. Neither the different surgical procedures nor atropine significantly altered plasma levels of secretin basally and in response to intestinal HCl. We conclude that 1) cholinergic fibers within the vagus nerves but not the splanchnic nerves are important mediators of the pancreatic bicarbonate response to low loads of HCl and 2) release of secretin by intestinal HCl is not under cholinergic and splanchnic control.


1983 ◽  
Vol 245 (1) ◽  
pp. G78-G84
Author(s):  
A. S. Fink ◽  
M. Luxenburg ◽  
J. H. Meyer

To study interactions between hydrochloric acid and fatty acids on pancreatic secretion, six dogs with chronic gastric, pancreatic, and small intestinal cannulas received various combinations of the following intestinal perfusates: 20, 40, and 80 mM hydrochloric acid, oleate, dodecanoate, or 0.15 M saline. Regional intestinal perfusion (a proximal segment measuring 45 cm from the pancreatic duct versus the remaining small bowel) was utilized to separate the aqueous acid and lipid solutions. Both oleate and dodecanoate augmented the bicarbonate output induced by intraluminal acidification. In other experiments, intraluminal oleate, when combined with exogeneous intravenous secretin (12.5-900 ng . kg-1 . h-1), potentiated the secretin-induced bicarbonate output at low secretin doses. Dodecanoate also increased secretin-induced bicarbonate output. In all of these studies, protein outputs were increased by intestinal fatty acids. It is concluded that intestinal fatty acids can enhanced acid-induced canine pancreatic secretion.


1990 ◽  
Vol 52 (2) ◽  
pp. 225-232 ◽  
Author(s):  
Koji TAKEUCHI ◽  
Hiromichi NIIDA ◽  
Masashi MINAMI ◽  
Susumu OKABE

2002 ◽  
Vol 103 (1) ◽  
pp. 96-99 ◽  
Author(s):  
Marissa Howard-McNatt ◽  
Aaron S. Fink
Keyword(s):  

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