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At least 217 records · Page 12Linked to original sources
PubMed1990

Sulphomucin-secreting intestinal metaplasia in the human gastric mucosa. An association with intestinal-type gastric carcinoma.

Sixty-three gastrectomy specimens (21 with early intestinal type carcinoma, 21 with early diffuse carcinoma, and 21 with benign nonneoplastic lesions) were examined histochemically to determine the distribution of intestinal metaplasia (IM), particularly the sulphomucin-secreting type (Type IIB IM). The frequency and distribution of Type IIB IM were similar, irrespective of the disease, when age of the patient was matched and if the extension of the IM was similar. Type IIB IM was usually observed in the mucosa along the lesser curvature of the lower portion of the stomach, particularly in elderly patients and was mainly located in the deeper foveolae and intermingled with or transient to those in other types of IM. These findings suggest that a casual relationship between Type IIB IM and intestinal type carcinoma is dubious.

Age Factors↗
PubMed1961

The stability of the radiotriolein bond in intestinal secretions.

The radiotriolein test has been reported to be unreliable in the diagnosis of steatorrhoea. A possible explanation is provided by these studies in which labelled triolein was incubated in human gastric juice, duodenal juice, and faeces; the bond was not stable on duodenal juice.

Celiac Disease↗
PubMed1987

Specific antibodies to cholera toxin in rabbit milk are protective against Vibrio cholerae-induced intestinal secretion.

Breast feeding helps to protect the nursing infant against infectious diarrhoeas, but the relative importance of antibodies compared with other components present in milk is unsettled. In order to aid in resolving this issue we evaluated the ability of milk, collected from rabbits not immunized or immunized enterally during pregnancy with toxinogenic, live Vibrio cholerae, to inhibit water secretion induced by V. cholerae in rat ileal loops. Non-immune milk was not inhibitory, whereas immune milk was. The inhibitory component of the immune milk was immunoglobulin by virtue of its molecular weight and absorption by an anti-rat immunoglobulin immunosorbent. In addition, the inhibitory antibodies were principally antibodies to cholera toxin because they could be removed from the milk by a cholera toxin immunosorbent but were only partially removed by incubation with whole V. cholerae. Thus, in rabbit milk, we could implicate specific antibodies in protection against intestinal water secretion induced by V. cholerae.

Animals↗
PubMed1998

Intestinal handling of mercury in the rat: implications of intestinal secretion of inorganic mercury following biliary ligation or cannulation.

Three sets of experiments were carried out to determine if there is an intestinal secretory component in the fecal excretion of administered inorganic mercury. In the first set of experiments the disposition of a nontoxic 0.5-micromol/kg intravenous dose of inorganic mercury was evaluated in control rats and rats whose bile duct had been ligated. Data collected 24 h after the administration of mercuric chloride indicated that some inorganic mercury had moved from the blood across the epithelium into the lumen of the stomach, small intestine, and large intestine. This secretory movement of mercury was most prominent in the small intestine. Interestingly, the renal uptake and accumulation of mercury were diminished significantly in the rats whose bile duct had been ligated. A time-course experiment showed that the maximum amount of secretory movement of mercury into the lumen of the small intestine occurred during the initial 12 h after the injection of mercuric chloride. By the end of 24 h after the injection of mercuric chloride, much of the inorganic mercury secreted in the small intestine appeared to have moved down into the large intestine. In a third experiment, the disposition of mercury was evaluated in control rats and rats who had their bile duct cannulated. The rationale for this third experiment was to study the disposition of mercury under conditions where obstruction of biliary outflow from the liver would not be as much of an issue as with ligation of the bile duct. Evidence for movement of mercury into the lumen of the intestines was also obtained from the rats whose bile duct had been ligated. Eighteen hours after the injection of mercuric chloride the amount of mercury in the luminal compartment of the small intestine was not statistically different between the two groups of rats. Approximately 1.7-2.1% of the administered dose was present in the luminal contents of the small intestine. Decreased renal uptake of mercury was also detected in the rats whose bile duct had been cannulated. The findings from the present study show that when bile flow is obstructed or diverted, clear evidence for secretory movement of mercury into the lumen of the gastrointestinal (GI) tract can be demonstrated. These findings also indicate that the secretory movement of mercury into the lumen of the GI tract is a mechanism that contributes significantly to the pool of mercury that is excreted in the feces.

Animals↗
PubMed1982

The effect of nicotinic and muscarinic receptor blockade on cholera toxin induced intestinal secretion in rats and cats.

The effects of hexamethonium (cholinergic nicotinic receptor antagonist) and atropine (cholinergic muscarinic receptor antagonist) on cholera toxin induced secretion were investigated in denervated segments of the small intestine of rats and cats. While there was no effect of atropine, hexamethonium markedly inhibited choleraic secretion and turned it into a net fluid absorption in many animals. This observation further strengthens our hypothesis that the enteric nervous system is involved in cholera secretion.

Animals↗
PubMed1982

Effects of epinephrine, clonidine, L-phenylephrine, and morphine on intestinal secretion mediated by Escherichia coli heat-stable enterotoxin in pig jejunum.

Perfusion of pig jejunum with Escherichia coli heat-stable enterotoxin (strain 1261) reversed net absorption of water and electrolytes to net secretion. Addition of the alpha-adrenergic agonists clonidine (5 X 10(-7) M) or L-phenylephrine (5 X 10(-6) M), or the opiate agonist morphine (3.6 X 10(-6) M) to the perfusate reduced the secretory response to enterotoxin and stimulated absorption in normal jejunum. Epinephrine (5 X 10(-5) M) did not stimulate absorption in controls but reduced chloride loss in the presence of enterotoxin. Mucosal sodium--potassium adenosine triphosphatase was unchanged but disaccharidase activity was decreased in the presence of enterotoxin. The results suggest that alpha-adrenergic agonists and opiate agonists may exert an antidiarrheal action by increasing net transport across intestinal epithelium.

Animals↗
PubMed1981

[Immunoglobulins A and G in the intestinal secretions of rats in different microbiologic conditions].

Experiments were made with 3 groups of inbred CDF (F344) Crl rats: 30 germ-free, 30 conventional and 18 germ-free animals infected orally with Shigella flexneri 2aN 516. Secretory IgA (S-IgA) was isolated from gut secretion of the conventional rats to obtain rabbit antiserum against it. The levels of S-IgA, IgA and IgG in blood serum and gut secretion were determined. It was shown that gut secretion of the germ-free rats contained no less S-IgA than that from the conventional rats, at the same time IgG was not found in the germ-free rats. After injection of the germ-free rats with Shigella flexneri the content of S-IgA in gut secretion did not rise but there appeared IgG which differed immunochemically from serum IgG2. Within the first week after the injection, gut secretion showed specific antibodies to Shigella flexneri, which was ascertained with the aid of the hemagglutination inhibition test. The titers of antibodies exceeded 1:4096 by day 21. Antibodies in serum appeared much later and in low titers (1:16, 1:32). Therefore, the local immune response was marked to a greater degree than the generalized one. In spite of the presence of specific antibodies in high titers, Shigella flexneri persisted in the hosts, i. e. one could observe a clinically normal bacterial carriage.

Animals↗
PubMed1983

Clostridium difficile toxin-induced intestinal secretion in rabbit ileum in vitro.

In rabbit ileum in vitro Clostridium difficile toxin (200 microliter crude extract) almost abolished net Na absorption, by decreasing mucosa to serosa flux, and induced net Cl secretion by increasing the serosa to mucosa flux. These flux changes were induced when there was no visible histological damage to the mucosa. The toxin did not influence adenylate or guanylate cyclase activity in a plasma membrane fraction of isolated rabbit enterocytes nor did it affect cAMP concentrations in intact rabbit ileum pre-incubated with toxin. The flux responses to the toxin were prevented by removing calcium from the serosal medium, suggesting that the secretory process may be calcium dependent. These results indicate a possible mechanism by which this toxin could induce diarrhoea.

Animals↗
PubMed2003

Contribution of serum immunoglobulin transudate to the antibody immune status of murine intestinal secretions: influence of different sampling procedures.

Serum immunoglobulin transudation into the murine gut after intragastric immunization with the model antigen ovalbumin and cholera toxin adjuvant was investigated with regard to the mucosal sampling technique applied. The levels of serum-derived immunoglobulin A (IgA) turned out to be lowest in feces, intermediate in gut lavage fluid specimens, and highest in filter wick-collected samples. However, these levels did not exceed 2% of total and specific IgA in any mucosal sample type, except after the administration of very high antigen doses (> or =1 mg of antigen per g of body weight), when transudation rates of up to 31% could be measured in filter wick-collected samples from individual animals. Luminal IgG was plasma transudate and/or bile borne and appeared to be reabsorbed at the mucosa to some extent.

Adjuvants, Immunologic↗
PubMed1996

Nitric oxide inhibits rat intestinal secretion by Clostridium difficile toxin A but not Vibrio cholerae enterotoxin.

BACKGROUND & AIMS: Intestinal inflammation is associated with increased synthesis of nitric oxide, whereas inhibition of NO synthase (NOS) reduces experimental chronic intestinal inflammation. The aim of this study was to test the effects of NO blockers and donors on acute intestinal inflammation induced by Clostridium difficile toxin A in rat ileum. METHODS: Rats received NOS inhibitors or NO donors before measurement of toxin-mediated ileal secretion and permeability changes. Mucosal mast cell and neutrophil activity were measured by release of rat mast cell protease II and myeloperoxidase activity, respectively. RESULTS: NOS inhibitors augmented but an NO donor inhibited toxin A-mediated ileal secretion and permeability when given before but not after toxin administration. Neither an NOS inhibitor nor an NO donor had any effect on cholera toxin-mediated secretion. Mast cell degranulation and neutrophil infiltration occurred after injection of toxin A or an NOS inhibitor, whereas the NO donor blocked both toxin A effects. CONCLUSIONS: NOS inhibitors augmented and an NO donor blocked the intestinal effects of toxin A but not of cholera toxin. NO protects against toxin A by inhibition of intestinal mast cells and neutrophils, which are activated by toxin A, but not by cholera toxin.

Acetylcysteine↗
PubMed1998

In vivo non-linear intestinal permeability of celiprolol and propranolol in conscious dogs: evidence for intestinal secretion.

The objective of this study was to investigate the absorption mechanism of celiprolol as a potential source of the drug's non-linear oral pharmacokinetics by determining its intestinal permeability as a function of concentration in vivo in dogs. Solutions of different celiprolol concentrations containing propranolol as an internal absorption marker were perfused through an isolated jejunal segment and samples were analyzed by an enantioselective HPLC method (Hartmann et al., J. Chromatogr., 496 (1989) 387-396). Permeability (P(eff) x 10(4) cm/s) of celiprolol increased significantly from 1.9-2.1 for the lower concentrations to 3.2 for the highest concentration, while the variability decreased. No statistical differences in the uptake between the two enantiomers were observed. Permeability of propranolol also increased significantly with increasing celiprolol concentrations, suggesting that propranolol might be utilizing the same carrier protein. In conclusion, the non-linear and variable oral pharmacokinetics of celiprolol might be due to a non-linear saturable, possibly secretion component in its uptake mechanism.

Animals↗
PubMed1978

Rat intestine secretes discoid high density lipoprotein.

High density lipoprotein was isolated from pooled rat serum and mesenteric lymph of lymph fistula rats. In most experiments, 5,5'-dithionitrobenzoic acid, an inhibitor of the enzyme lecithin:cholesterol acyltransferase, was added during the collection of lymph to prevent modification of the lipid composition of newly secreted lipoproteins. Negative staining electron microscopy of lymph high density lipoprotein revealed discoidal particles (190+/-3 x 55+/-1 A) which tended to form rouleaux, smaller spherical particles were also present. Serum high density lipoprotein contained only spherical particles (diameter 93+/-4 A). Lipid analysis showed that lymph high density lipoprotein was enriched in phospholipid and deficient in cholesterol esters when compared to serum high density lipoprotein. The phospholipid to cholesterol esters ratio was greatest in basal lymph high density lipoprotein when compared to fatty lymph and serum high density lipoprotein. From analysis of the lipid compositional data and direct particle measurement by electron microscopy, it could be determined that congruent with50% of basal lymph high density lipoprotein and 30% of fatty lymph high density lipoprotein was discoid. Basal lymph high density lipoprotein was enriched in apoA-I and deficient in the arginine-rich peptide, and the apoprotein composition of fatty lymph high density lipoprotein more closely resembled serum. These observations demonstrate that intestinal lymph contains two types of high density lipoprotein particles, a discoid nascent particle deficient in cholesterol ester and rich in apoA-I, and spherical high density lipoprotein derived from plasma. A significant amount of lymph high density lipoprotein appears to be secreted by the intestine.

Animals↗
PubMed1987

Azodisalicylate (azodisal sodium) causes intestinal secretion. Comparative study of the effect of azodisalicylate, sulfasalazine, 5-aminosalicylic acid and sulfapyridine on the water and electrolyte transfer and the morphology of the rat ileum and colon in vivo.

Azodisalicylate (ADS) is one of the possible successors of sulfasalazine in the treatment of ulcerative colitis. The following results were obtained when comparing the influence of ADS on net water and electrolyte transfer in tied-off loops of the rat ileum and colon in vivo with sulfsalazine, 5-aminosalicylic acid, and sulfapyridine. (1) Sulfasalazine, 5-aminosalicylic acid and sulfapyridine had no effect on water and electrolyte transfer of the healthy intestinal mucosa in concentrations up to 400 mg%. (2) ADS showed a concentration-dependent inhibition effect on net water, sodium and chloride absorption and stimulated secretion at concentrations higher than 100 mg%. (3) No morphological alterations of the mucosa could be observed by light and transmission electron microscopy. The observed effect of ADS might have some clinical significance in patients with a decreased absorptive capacity of the colon in ulcerative colitis, in contrast to healthy volunteers, where the high absorptive capacity of the colon might compensate the decreased absorption or stimulated secretion in the small intestine.

Aminosalicylic Acids↗
PubMed1988

Stimulation of intestinal secretion of apolipoprotein AI by triiodothyronine.

Rats were made hyperthyroid with triiodothyronine in an osmotic minipump implanted intraperitoneally for one week. Intestinal lymph was collected from euthyroid and hyperthyroid rats for 40-55 hours. The rate of apolipoprotein AI (apo AI) secreted into the lymph by hyperthyroid rats exceeded that of euthyroid rats (149 +/- 9 vs 95 +/- 2 micrograms/hr), and was not associated with a proportional increase in the output of triglyceride. The fall in plasma concentration of apoAI in the euthyroid (10 mg/dl) and hyperthyroid (23 mg/dl) could be accounted for by the loss due to diversion of lymph. It appears that the intestine may contribute significantly to the increased plasma levels of apoAI observed in the hyperthyroid rats.

Animals↗