Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INTESTINAL SECRETIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1979

Inhibition of PGE1 induced intestinal secretion by the synthetic enkephalin analogue FK 33-824.

1. The effects of the enkephalin analogue, FK 33-824 were compared with those of morphine and naloxone on the prostaglandin E1-induced increase in intestinal fluid volume and unanaesthetized and pithed rats. 2. FK 33-824 inhibits the prostaglandin E1-induced increase in intestinal fluid volume both in unanaesthetized and pithed rats. 3. Naloxone abolished the inhibitory effect of FK 33-824 in both experimental models. 4. It can be concluded from the experiments in pithed rats that the inhibitory effect of FK 33-824, like that of morphine, on prostaglandin E1-induced secretion is caused by a peripheral action. 5. It is assumed that endogenous enkephalins protect against prostaglandin-mediated loss of fluid into the gut lumen. This protective effect can be mimicked by an enkephalin analogue and blocked by naloxone.

Animals↗
PubMed1986

Physiological role of somatostatin in the digestive tract: gastric acid secretion, intestinal absorption, and motility.

Somatostatin is found in both endocrine cells and nerve fibres of the gastrointestinal tract and has several inhibitory effects on the digestive tract. Somatostatin is a potent inhibitor of gastrin release; its secretion is regulated predominantly by the cholinergic pathway, which inhibits somatostatin and thus stimulates gastrin release. Gastric acid secretion is inhibited by both the paracrine and circulating peptide (hormonal) effects of somatostatin. Somatostatin secretion is a direct effect of acid on the somatostatin cell, since it is unaffected by the axonal blocker tetrodotoxin. Somatostatin antiserum eliminates the inhibitory effect of somatostatin and thus augments acid secretion. It therefore appears that somatostatin plays a physiological role in regulating gastric acid secretion, and it is possible that a lack of the inhibitory function of somatostatin is an aetiological factor in peptic ulcer disease. Postprandially, a rise in serum somatostatin concentration occurs which is twice as high with protein and fat as it is with carbohydrates. Several studies have shown that somatostatin inhibits nutrient absorption, indicating that somatostatin might be a physiological regulator in the homeostasis of ingested nutrients by modulating the intestinal absorption rate. Experiments have also demonstrated that somatostatin infusion inhibits intestinal motility; the interval between migrating myoelectric complexes is increased, and transit time is increased.

Animals↗
PubMed2001

Active intestinal secretion of new quinolone antimicrobials and the partial contribution of P-glycoprotein.

Transport of quinolone antimicrobials and the contribution of the secretory transporter P-glycoprotein were studied in-vivo and in-vitro. In rat intestinal tissue (Ussing chambers method) and human Caco-2 cells (Transwell method), grepafloxacin showed secretory-directed transport. In both experimental systems, the secretory-directed transport was decreased by ciclosporin A, an inhibitor of P-glycoprotein, and probenecid, an inhibitor of anion transport systems. This suggested the contribution of P-glycoprotein and anion-sensitive transporter(s). The involvement of P-glycoprotein was investigated by using a P-glycoprotein over-expressing cell line, LLC-GA5-COL150, and P-glycoprotein-gene-deficient mice (mdr1a(-/-)/1b(-/-) mice). LLC-GA5-COL150 cells showed secretory-directed transport of grepafloxacin, while the parent cell line, LLC-PK1, did not. The secretory-directed transport of sparfloxacin and levofloxacin was also detected in LLC-GA5-COL150 cells. In the mdr1a(-/-)/1b(-/-) mice, the intestinal secretory clearance was smaller than that in wild-type mice after intravenous administration of grepafloxacin. Moreover, the absorption from an intestinal loop in mdr1a(-/-)/1b(-/-) mice was larger than that in wild-type mice. Accordingly, it appears that some quinolones are transported by secretory transporters, including P-glycoprotein. The involved transporters function in-vivo not only to transport grepafloxacin from blood to intestine but also to limit its intestinal absorption.

ATP Binding Cassette Transporter, Subfamily B↗
PubMedDate not supplied

Absence of intestinal secretion on supernatants from macrophages stimulated with Clostridium difficile toxin B on rabbit ileum.

Several studies have documented the involvement of both Clostridium difficile, toxins, A and B in the pathogenesis of antibiotic-associated diarrhea. Recently, we demonstrated that IL-1 beta is the intestinal secretory factor released by macrophages stimulated with toxin A. The aim of this study was to evaluate the importance of macrophages stimulated with toxin B on rabbit ileal ion transport. The changes in ion transport were analyzed by studying the short-circuit current of the rabbit ileal mucosa mounted in Ussing chambers. The supernatants of macrophages treated with toxin B (3.6 x 10(-7) M) had no effect on the ion transport (change in short-circuit current =28.0+/-9.2 vs. control=26.8+/-3.6 microA cm(-2)). Supernatants of macrophages stimulated with toxin A (3.2 x 10(-7) M), our positive control, induced a significant change in ileal ion transport (delta I(sc)=55.2+/-5.7 mA cm(-2)). It was also observed that, like toxin A, toxin B stimulated macrophages to produce TNF-alpha (555.0+/-37.9 pg/ml vs. control=182.0+/-39.8 pg/ml; p<0.05). Nevertheless, in contrast to toxin A, toxin B did not stimulate IL-1 beta synthesis (28.0+/-7.5 pg/ml vs. control=40. 0+/-14.4 pg/ml; p>0.05). We conclude that the supernatants of macrophages stimulated with toxin B are not able to stimulate ion transport and that both toxins stimulate the genesis of TNF-alpha, but only toxin A induces the synthesis of IL-1 beta, which, we have earlier reported, causes an electrogenic intestinal response in rabbit ileum.

Animals↗
PubMed1979

PGE1-induced intestinal secretion: mechanism of enhanced transmucosal protein efflux.

The effects of local intra-arterial prostaglandin E1 (PGE1) infusion on net transmucosal volume and protein fluxes, lymphatic volume and protein fluxes, and regional hemodynamics were ascertained in autoperfused segments of cat ileum. After acquiring control values (and tissue samples) for the various parameters, PGE1 (5.0 microgram/min) was infused directly into the superior mesenteric artery. The PGE1 infusions resulted in dramatic increases in ileal lymphatic volume and protein fluxes and blood flow. Infusion of PGE1 caused a reversion of net mucosal volume absorption to net secretion and an increased loss of plasma proteins into the lumen. Ultrastructural analysis of tissue samples taken during the PGE1 infusion indicate major structural damage to the mucosal membrane. The physiological and ultrastructural data acquired in this study suggest that 1) the increased transmucosal protein efflux during intra-arterial PGE1 infusions results from an alteration in mucosal transcapillary fluid exchange and 2) a significant portion of PGE1-induced ileal secretion is passively mediated.

Animals↗
PubMed1989

Serotonin and substance P stimulate intestinal secretion in the isolated perfused ileum.

The actions of serotonin and substance P have been examined with use of an isolated, vascularly perfused rabbit ileal preparation. The vascular perfusate was composed of a modified Krebs' buffer solution that contained washed human red blood cells (hematocrit, 15% to 20%) and 3% albumin, with no added hormones or peptides. Ileal blood flow was held constant at 49.3 +/- 3.1 ml/min per 100 gm wet weight of intestine. Net intestinal water and electrolyte fluxes were calculated by means of an isosmotic buffer that contained carbon-14 polyethylene glycol as a nonabsorbable volume marker. Viability of this isolated perfused ileal preparation was confirmed on the basis of light microscopy, oxygen consumption, and transmucosal potential difference measurements. Control experiments, without exogenous hormone infusion, resulted in a stable preparation with a basal secretory state. Intra-arterial serotonin at 2.5 micrograms/min (n = 10) significantly stimulated secretion of H2O, Na+, and Cl- (p less than 0.01). Intra-arterial substance P at 2.5 x 10(-1) micrograms/min (n = 7) significantly increased the secretion of H2O, Na+, and Cl- (p less than 0.02). The dose of serotonin was designed to yield serotonin levels that resembled those found circulating in patients with carcinoid syndrome. These data indicate that serotonin and substance P are potent secretagogues in a mammalian system, independent of their effect on mesenteric blood flow and in the absence of extra-intestinal hormonal and neural influences.

Animals↗