Absence of Na+–H+ barrier function in mucosa of canine small bowel

1978 ◽  
Vol 56 (4) ◽  
pp. 617-623 ◽  
Author(s):  
Darlene G. Kelly ◽  
Charles F. Code

The study was designed to determine whether the special Na+–H+ barrier function or the gastric mucosa is present in the mucosa of the small bowel and whether a gastric mucosal barrier breaker (hexanoic acid) would accelerate the fluxes of sodium in duodenum–jejunum and ileum as in the stomach. The observations were made in healthy conscious dogs with Thiry-Vella fistulae of the small bowel or Heidenhain pouches of the gastric corpus. These barrier characteristics of the stomach were completely absent in the small intestine where bidirectional Na fluxes were 5–10 times greater than in the stomach and were not accelerated by hexanoic acid as they were in the stomach.A comparison was made between the rates of absorption of hexanoic acid, sodium hexanoate, and HCl from the pouches and fistulae. The lipid-soluble fatty acid was transported at all sites more rapidly than its water-soluble sodium salt. In the stomach and ileum the H+ of HCl and sodium hexanoate were absorbed at similar slow rates. The duodenal–jejunal mucosa, however, transported H+ at rates nearly identical to those of hexanoic acid. In our tests HCl was not neutralized in duodenal contents while large quantities were neutralized in the contents of ileum.

1977 ◽  
Vol 232 (1) ◽  
pp. E44
Author(s):  
A K Mukhopadhyay ◽  
P J Thor ◽  
E M Copeland ◽  
L R Johnson ◽  
N W Weisbrodt

The effect of cholecystokinin on the myoelectric activity of the small intestine was determined in conscious dogs. Six animals were implanted with electrodes along the small intestine, and a cannula was placed in the stomach. A second cannula was inserted into the duodenum in three animals, and a pancreatic fistula was prepared in three animals. Recordings were made in the fasted state, during the intravenous infusion of either saline or cholecystokinin-octapeptide (CCK-OP), during the intraduodenal infusion of either saline or L-tryptophan, and during the fed state. CCK-OP disrupted the fasted pattern of myoelectric activity, caused a dose-dependent increase in spike potentials, and caused a dose-dependent increases in pancreatic protein secretion. Stimulation of myoelectric activity occurred at doses that produced submaximal protein secretion; however, the stimulation was not identical to that seen with feeding. Intraduodenal infusion of L-tryptophan increased pancreatic protein secretion, interrupted the fasted pattern of motility, and induced a pattern similar to that seen with feeding. We conclude that CCK alters small intestinal motility and may play a role in the changes in small-bowel motility caused by the ingestion of food.


2002 ◽  
Vol 34 (3) ◽  
pp. 926-928 ◽  
Author(s):  
A.R. Mueller ◽  
A. Pascher ◽  
R.J. Schulz ◽  
N. Rayes ◽  
K.P. Platz ◽  
...  

2003 ◽  
Vol 124 (4) ◽  
pp. A315
Author(s):  
Peter Suenaert ◽  
Veerle Bulteel ◽  
Willy Van Driessche ◽  
Paul Rutgeerts

1993 ◽  
Vol 105 (2) ◽  
pp. 340-346 ◽  
Author(s):  
Yasuhiro Nishizaki ◽  
Paul H. Guth ◽  
Jonathan D. Kaunitz

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 78-78
Author(s):  
Ming Qi ◽  
B I E Tan ◽  
Yulong Yin ◽  
Simeng Liao ◽  
Jianjun Li ◽  
...  

Abstract The piglets with postnatal growth retardation (PGR) have high mortality and morbidity during their growth and development. Abnormal development of small intestine is casually implicated in impaired growth, but the exact mechanism still remains poorly understood. Thus, the present study investigated the immune profiles related to intestinal mucosal barrier in PGR and healthy piglets. The plasma sample, middle segments of small intestine, and the intestinal mucosa were obtained from healthy and PGR piglets at 42d of age. Compared to healthy piglets, higher plasma concentrations of diamine oxidase and D-lactate were observed in PGR piglets (P < 0.05). Decreased villous height, ratio of villous height to crypt depth, as well as sparse villi, jagged microvilli were also found in jejunum and ileum of PGR piglets. PGR also decreased the percentage of proliferating cell nuclear antigen (PCNA)-positive cells, as well as abundance of Zonula occludens-1, Occludin, Claudin-1, and E-cadherin mRNA and protein in jejunal and ileal mucosa (P < 0.05). The lower concentration of sIgA in jejunal mucosa, and lysozyme in both jejunal and ileal mucosa, but higher level of β-defensins in the ileal mucosa were observed in PGR piglets as compared to healthy piglets (P < 0.05). The percentage of CD68-positive cells were significantly increased, but the levels of P-glycoprotein were decreased in jejunum and ileum from PGR piglets (P < 0.01). Moreover, the expression of proteins involved in p38 MAPK/NF-kB pathway was significantly upregulated in jejunal and ileal mucosa from PGR piglets (P < 0.05). Collectively, these results indicated that the PGR piglets exhibited impaired intestinal integrity, and decreased capacity of mucosal immune function, which may result in severe inflammatory response via the activation of p38 MAPK/NF-kB pathway. Our findings may have important implications in the prevention and treatment of the intestinal mucosal barrier dysfunction in piglets.


2000 ◽  
Vol 32 (6) ◽  
pp. 1275-1277 ◽  
Author(s):  
A.R Mueller ◽  
K.-P Platz ◽  
A Schirmeier ◽  
N.C Nüssler ◽  
D Seehofer ◽  
...  

2012 ◽  
Vol 109 (4) ◽  
pp. 667-677 ◽  
Author(s):  
Aude Bressenot ◽  
Shabnam Pooya ◽  
Carine Bossenmeyer-Pourie ◽  
Guillaume Gauchotte ◽  
Adeline Germain ◽  
...  

Dietary methyl donors and their genetic determinants are associated with Crohn's disease risk. We investigated whether a methyl-deficient diet (MDD) may affect development and functions of the small intestine in rat pups from dams subjected to the MDD during gestation and lactation. At 1 month before pregnancy, adult females were fed with either a standard food or a diet without vitamin B12, folate and choline. A global wall hypotrophy was observed in the distal small bowel (MDD animals 0·30 mm v. controls 0·58 mm; P< 0·001) with increased crypt apoptosis (3·37 v. 0·4 %; P< 0·001), loss of enterocyte differentiation in the villus and a reduction in intestinal alkaline phosphatase production. Cleaved caspase-3 immunostaining (MDD animals 3·37 % v. controls 0·4 %, P< 0·001) and the Apostain labelling index showed increased crypt apoptosis (3·5 v. 1·4 %; P= 0·018). Decreased proliferation was observed in crypts of the proximal small bowel with a reduced number of minichromosome maintenance 6 (MDD animals 52·83 % v. controls 83·17 %; P= 0·048) and proliferating cell nuclear antigen-positive cells (46·25 v. 59 %; P= 0·05). This lack of enterocyte differentiation in the distal small bowel was associated with an impaired expression of β-catenin and a decreased β-catenin–E-cadherin interaction. The MDD affected the intestinal barrier in the proximal small bowel by decreasing Paneth cell number after immunostaining for lysosyme (MDD animals 8·66 % v. controls 21·66 %) and by reducing goblet cell number and mucus production after immunostaining for mucin-2 (crypts 8·66 v. 15·33 %; villus 7 v. 17 %). The MDD has dual effects on the small intestine by producing dramatic effects on enterocyte differentiation and barrier function in rats.


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