scholarly journals Sulphur Metabolism and Excretion Studies in Ruminants VII. Secretion of Sulphur and Nitrogen in Sheep Pancreatic and Bile Fluids

1972 ◽  
Vol 25 (4) ◽  
pp. 817 ◽  
Author(s):  
PR Bird

[35S]taurine or [35S]Na2S04 was given as a single intraduodenal infusion and the combined bile and pancreatic (OBD) secretions continuously collected, sampled, and returned. In two sheep 41-51 % of 35S from [35S]taurine was recovered in OBD fluids, less than 1 % in the faeces, and less than 4 % in the urine, over 3 days. When the 35S-labelled OBD fluids were infused an estimated 90-113% of the 35S was recycled; in 6 days less than 2% was excreted in faeces and less than 4% in the urine. With other sheep 6-8% of 35S from [35S]Na2S04 was recovered in the OBD fluids and 63-76% in the urine over 4-5 days. When the 35S-labelled OBD fluids were infused 14--29% of the 35S was recycled.

1971 ◽  
Vol 24 (4) ◽  
pp. 1329 ◽  
Author(s):  
PR Bird

A basal ration containing 0�86 g sulphur was fed daily to sheep receiving a continuous intraruminal or intraduodenal infusion supplying 0-6 g sulphur, as sodium sulphate, per day.


1992 ◽  
Vol 262 (1) ◽  
pp. G35-G43 ◽  
Author(s):  
G. Sun ◽  
T. M. Chang ◽  
W. J. Xue ◽  
J. F. Wey ◽  
K. Y. Lee ◽  
...  

The release of cholecystokinin (CCK) and secretin into both circulation and duodenal lumen, after intraduodenal perfusion with sodium oleate or oral ingestion of fat, was studied in anesthetized and conscious dogs, respectively. Intraduodenal infusion with sodium oleate (4 mmol.kg.-1.h-1, pH 9.5) in anesthetized dogs with diversion of bile and pancreatic juice stimulated the release of both CCK and secretin not only into the circulation but also into the duodenal lumen. The concentration of CCK and secretin in the luminal perfusate increased from 0.2 +/- 0.1 to 2.1 +/- 0.4 nM and 0.34 +/- 0.16 to 2.59 +/- 0.63 nM, respectively. Intraduodenal infusion of NaHCO3 solution at pH 9.5 did not result in release of either hormone. Luminal release of both hormones was also observed by intraduodenal infusion of sodium oleate in the dogs without diversion of bile and pancreatic juice, albeit at lower concentrations than those released in the dogs with diversion. Analysis of the molecular form of luminal secretin by gel filtration, ion-exchange chromatography, and high-performance liquid chromatography showed only a single form of secretin with molecular size, hydrophobicity, and charge similar to those of natural porcine secretin. In contrast, multiple forms of CCK were released into both circulation and duodenal lumen with CCK-58 as the predominant form. In conscious dogs, CCK-58 was also found to be the predominant form of CCK released into the circulation after oral ingestion of fat.(ABSTRACT TRUNCATED AT 250 WORDS)


1926 ◽  
Vol 23 (8) ◽  
pp. 764-765 ◽  
Author(s):  
F. C. Koch ◽  
H. Sugata
Keyword(s):  

1999 ◽  
Vol 276 (6) ◽  
pp. G1501-G1506 ◽  
Author(s):  
Yuan-Xu Lu ◽  
Chung Owyang

In this study, we used an in vivo anesthetized rat model to investigate the mechanisms responsible for duodenal acid-induced inhibition of gastric motility. Intraduodenal infusion of HCl produced a rate-dependent decrease in intragastric pressure. Infusion of HCl at 2 ml/h produced a physiological plasma secretin level and elicited a decrease in intragastric pressure of 3.0 ± 0.2 cmH20. Infusion of rabbit secretin antiserum reduced the acid-induced inhibition of gastric motility by 85 ± 5%, suggesting mediation mainly by endogenous secretin. Administration of the cholecystokinin (CCK)-A antagonist MK-329 caused only a modest 10 ± 3% reduction in gastric relaxation, whereas the serotonin antagonist ICS-205930 had no effect. In contrast, immunoneutralization with the secretin antibody caused only a 15% reduction in the relaxation evoked by a higher rate of HCl infusion (3 ml/h), whereas MK-329 and ICS-205930 caused a 20 ± 4% reduction and no reduction, respectively. Bilateral truncal vagotomy or perivagal application of capsaicin completely abolished gastric relaxation in response to low rates (1–2 ml/h) of 0.1 N HCl infusion but only partially affected gastric relaxation in response to a higher infusion rate (3 ml/h). These observations indicate that multiple pathways mediate the duodenal acid-induced inhibition of gastric motility. At low rates of HCl infusion, gastric relaxation is mediated primarily by endogenous secretin, which acts through vagal afferent pathways. At higher rates of HCl infusion, gastric relaxation is mediated by endogenous secretin, CCK, and possibly by the direct action of HCl on vagal afferent pathways or yet unidentified neuropathways.


1972 ◽  
Vol 25 (1) ◽  
pp. 185 ◽  
Author(s):  
PR Bird

The concentrations of volatile sulphides in the rumen fluid of sheep were determined at intervals after giving single intraruminal infusions of DL-methionine, L-cystine, or L-cysteine. The basal ration fed contained 0�1 % sulphur.


2001 ◽  
Vol 281 (3) ◽  
pp. R753-R759 ◽  
Author(s):  
Takashi Doi ◽  
Min Liu ◽  
Randy J. Seeley ◽  
Stephen C. Woods ◽  
Patrick Tso

We determined apolipoprotein AIV (apo AIV) content in intestinal epithelial cells using immunohistochemistry when leptin was administered intravenously. Most of the apo AIV immunoreactivity in the untreated intestine was located in the villous cells as opposed to the crypt cells. Regional distribution of apo AIV immunostaining revealed low apo AIV content in the duodenum and high content in the jejunum that gradually decreases caudally toward the ileum. Intraduodenal infusion of lipid (4 h) significantly increased apo AIV immunoreactivity in the jejunum and ileum. Simultaneous intravenous leptin infusion plus duodenal lipid infusion markedly suppressed apo AIV immunoreactivity. Duodenal lipid infusion increased plasma apo AIV significantly (measured by ELISA), whereas simultaneous leptin infusion attenuated the increase. These findings suggest that leptin may regulate circulating apo AIV by suppressing apo AIV synthesis in the small intestine.


1976 ◽  
Vol 230 (3) ◽  
pp. 784-789 ◽  
Author(s):  
KY Lee ◽  
HH Tai ◽  
WY Chey

In five conscious dogs with gastric fistula and two duodenal cannulas, plasma RIA secretin and gastrin levels were determined in response to 1) infusion of 0.1 N HCl in the proximal duodenal cannula, 2) ingestion of a meal, and 3) intraduodenal infusion of 0.1 N HCl following ingestion of a meal. Significant increases in plasma RIA secretin levels occurred during duodenal acidification. However, no significant change occurred in the secretin levels after ingestion of a meal, whereas significant increase in plasma gastrin level was observed. Postprandial duodenal pH remained above 4.5 for 3 h.


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