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Results for “INTESTINAL SECRETIONS”

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At least 109 records · Page 6Linked to original sources
PubMed1982

Effect of administration of activated charcoal and fibre on absorption, excretion and steady state blood levels of digoxin and digitoxin. Evidence for intestinal secretion of the glycosides.

The effects of activated charcoal and fibre on absorption and stationary plasma levels of digoxin and digitoxin have been studied. The effect of fibre alone is small but an interactive effect on absorption may occur if fibre and digoxin are ingested simultaneously. Charcoal effectively decreases glycoside absorption even when administered after the glycosides. During maintenance therapy with digoxin or digitoxin, charcoal administration decreased the glycoside plasma levels by 31.2% and 18.3% respectively. It is suggested that even digoxin may have a significant biliary excretion and enterohepatic circulation or that this glycoside has a significant intestinal secretion. The therapeutic implication of this study is that charcoal may be of value, not only in the management of acute glycoside poisoning, but also in some cases of more chronic intoxication.

Adult↗
PubMed1999

[The meaning of gastric secretion intestinal phase disorders in the pathogenesis of ulcers and their surgical correction].

The data concerning the disorder of the gastric secretion intestinal phase in patients with complicated forms of ulcer disease and with recurrent ulcer as well are presented. The mechanism was shown, which if noneliminated can cause nonfavourable result of the operation performed for the ulcer disease complications. The data presented trust the necessity of more meticulous studying of disorders of the gastric acidproducing intestinal phase in surgical gastroenterology.

Duodenogastric Reflux↗
PubMed1984

The involvement of the enteric nervous system in the intestinal secretion evoked by cyclic adenosine 3'5'-monophosphate.

Intestinal fluid secretion was evoked in vivo in rats and cats by introducing dibutyrylcyclic adenosine 3,5-monophosphate (db-cAMP) or theophylline, a phosphodiesterase inhibitor, in the intestinal lumen. The intestines were denervated periarterially. It was demonstrated that three compounds of varying chemical structure and with different modes of action on nerves (tetrodotoxin, lidocaine, hexamethonium) decreased the secretory response 60-70%. It is concluded that the secretion induced by increasing the intracellular cAMP concentrations is in part evoked via the enteric nervous system.

Animals↗
PubMed1985

Effect of antigen form on local immunoglobulin A memory response of intestinal secretions to Shigella flexneri.

An enhanced memory response, as shown by increased titers of specific immunoglobulin A (IgA), was seen in intestinal secretions from isolated Thiry-Vella loops in rabbits primed orally with live, locally invasive Shigella sp. X16 and challenged 60 days later with a single oral dose of the same antigen. Heat-killed shigella preparations, when used as either the priming or challenge antigen, did not elicit such a memory response in this system. In the present study, the role of antigen form and dosage in eliciting the enhanced local IgA response was investigated. A noninvasive strain, Shigella flexneri 2457-0, was capable of significantly enhancing the mucosal IgA memory response, whereas heat-killed Shigella sp. X16 was unable to augment the local IgA response, even when the priming dose was increased 100-fold. A proposed mucosal adjuvant, DEAE-dextran, given orally with live Shigella sp. X16, did not enhance the local IgA response. Viable, noninvasive shigellae were effective priming agents in enhancing the local IgA memory response. The poor mucosal response to heat-killed shigella preparations is thought to be related to an ineffective delivery of nonviable bacterial antigens into gut-associated lymphoid tissues. The ability of the live, noninvasive strain to elicit a vigorous local IgA memory response when given orally to rabbits was consistent with previous findings that live preparations elicit the best mucosal IgA response.

Animals↗
PubMed1997

Mice lacking the guanylyl cyclase C receptor are resistant to STa-induced intestinal secretion.

Heat-stable enterotoxin (STa) is an important causative agent of diarrheal disease throughout the world. STa is known to bind specifically to receptors in the intestine, provoking intense intestinal secretion. Binding of STa, or of the mammalian endogenous ligands guanylin and uroguanylin, activates the guanylyl cyclase C receptor (GC-C); the resulting elevation of cGMP levels stimulates chloride secretion via CFTR. We have generated knockout mice which completely lack the GC-C receptor. These mice are viable and show no obvious alteration in intestinal fluidity. However, GC-C null mice are refractory to the secretory action of STa, proving that the GC-C receptor is necessary for the diarrheal response induced by STa.

Amino Acid Sequence↗
PubMed2000

Inhibition of small intestinal secretion by cannabinoids is CB1 receptor-mediated in rats.

We tested the hypothesis that cannabinoids, acting via a neuronal mechanism of action decrease small intestinal secretion. In vitro electrical stimulation induced ileal secretion in rats, that was attenuated by a cannabinoid receptor agonist, WIN 55212-2, (mesylate(R)-(+)-[2, 3-dihydro-5-methyl-3-[4-morpholino)methyl]pyrrolo-[1,2,3-de]-1, 4-benzoxazin-6-yl](1-naphthyl)methanone) but not its optical isomer WIN 55212-3. The inhibition of secretion induced by WIN 55212-2 was reversed by SR141716A (N-(piperidin-1-yl)-5-(4-chlorophenyl)-1(2, 4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride), a cannabinoid CB1 receptor antagonist. An ileal secretory response stimulated by acetylcholine was unaffected by WIN 55212-2. These findings show that cannabinoids inhibit neurally mediated secretion via cannabinoid CB1 receptors. Thus, cannabinoids may have therapeutic potential for diarrhea unresponsive to available therapies.

Acetylcholine↗
PubMed1979

Role of Ca(2+)-dependent regulator protein in intestinal secretion.

AFTER exposure to secretagogues the small intestine changes from a tissue that absorbs fluid and electrolyte from lumen to blood into a tissue that secretes electrolyte and fluid into the lumen(1-4). It has been shown that this secretion results from an increase in the passive Cl(-) permeability of the mucosal border, which permits Nad to leak passively from the lateral intercellular spaces, where it is present at hypertonic concentrations(5), into the mucosal bathing solution. Na(+) and water, electroosmotically coupled to Na(+) movement, leak through the tight junctions(1,2), and Cl(-) leaks through relatively anhydrous anion-selective channels, induced withira the mucosal border by secretagogues. The increased reflux of NaCl from the lateral intercellular space accounts for both the apparent decrease in electroneutral NaCl uptake across the mucosal border induced by secretagogues and the apparent increase in active CP secretion and short-circuit current(3,6,7). We have investigated the mechanism by which intestinal secretagogues increase passive Cl(-) permeability and thereby cause secretion. Cl(-) permeability is increased by several secretagogues, some of which, such as theophylline and choleragen, increase intracellular cyclic AMP concentration, and others, such as A23187, the Ca(2+) ionophore, or carbachol, do not(8). Thus there has been no known common mode of secretory induction. To investigate this problem we used two drugs that prevent intestinal secretion in vitro, RMI 12330A (Richardson Merrell), and the antipsychotic pheno-thiazine trifluoperazine (Stelazine, Smith, Kline and French). RMI 12330A prevents secretion by inhibiting choleragen-induced adenylyl cyclase activity(9). Stelazine inhibits phosphodiesterase in tissues(11,12) by preventing the activation of the enzyme by Ca(2+)-dependent regulator protein, CDR. We report here that it also inhibits Cl(-) secretion and binds to CDR.

Journal Article↗
PubMed1980

Intestinal secretion of digoxin in the rat. Augmentation by feeding activated charcoal.

Secretion of tritium-labeled digoxin was studied in rats using noneverted gut sacs, in ligated and perfused intestinal preparations in bile duct ligated rats, and by measuring 4 day fecal excretion of total radioactivity in bile duct ligated rats. Serosal to mucosal transfer was proportional to substrate concentration in vitro. In ligated intestinal loops radioactivity was concentrated in the lumen relative to serum. In perfused intestinal preparations the fraction of dose increased with time and was similar over a 100-fold range of doses. Bile duct ligated rats excreted 13.4 +/- 5.8 (S.D.) % of parenterally administered label in 4 day stool collections. Bile duct ligated rats treated with p.o. activated charcoal excreted significantly more radioactivity (33.4 +/- 7.9%). The results suggest that net nonbiliary intestinal secretion of digoxin and metabolites can be augmented by intraluminal binding. A role for this phenomenon in accounting for some effects of diseases and drug interactions is suggested.

Animals↗
PubMed2005

Recurrent networks of submucous neurons controlling intestinal secretion: a modeling study.

Secretomotor neurons, immunoreactive for vasoactive intestinal peptide (VIP), are important in controlling chloride secretion in the small intestine. These neurons form functional synapses with other submucosal VIP neurons and transmit via slow excitatory postsynaptic potentials (EPSPs). Thus they form a recurrent network with positive feedback. Intrinsic sensory neurons within the submucosa are also likely to form recurrent networks with positive feedback, provide substantial output to VIP neurons, and receive input from VIP neurons. If positive feedback within recurrent networks is sufficiently large, then neurons in the network respond to even small stimuli by firing at their maximum possible rate, even after the stimulus is removed. However, it is not clear whether such a mechanism operates within the recurrent networks of submucous neurons. We investigated this question by performing computer simulations of realistic models of VIP and intrinsic sensory neuron networks. In the expected range of electrophysiological properties, we found that activity in the VIP neuron network decayed slowly after cessation of a stimulus, indicating that positive feedback is not strong enough to support the uncontrolled firing state. The addition of intrinsic sensory neurons produced a low stable firing rate consistent with the common finding that basal secretory activity is, in part, neurogenic. Changing electrophysiological properties enables these recurrent networks to support the uncontrolled firing state, which may have implications with hypersecretion in the presence of enterotoxins such as cholera-toxin.

Action Potentials↗
PubMed1993

Modulation of small-intestinal secretion and absorption in chronic vitamin E deficiency: studies in rat jejunum in vitro.

1. A vicious cycle of malabsorption and malnutrition has been implicated in the pathogenesis of protracted diarrhoeal disease in infancy. Vitamin E deficiency is common in malnourished infants with protracted diarrhoea. We have studied the effects of chronic vitamin E deficiency on small-intestinal secretion and absorption in the rat. 2. Weanling rats were fed vitamin E-sufficient or -deficient diets for 21 weeks. Jejunal function was studied in vitro in an Ussing chamber after this period. 3. Steady-state isotopic flux experiments in unstimulated tissues demonstrated net Na+ and Cl- secretion in vitamin E-deficient jejuna but net Na+ and Cl- absorption in vitamin E-sufficient jejuna. 4. Basal intestinal short-circuit current was the same in both groups. 5. Cyclic nucleotide and maximal non-neuronal acetylcholine-mediated electrogenic secretion were increased in vitamin E-deficient jejuna. 6. Exogenous 5-hydroxytryptamine (serotonin) induced a smaller increment in electrogenic secretion in vitamin E-deficient jejuna. 7. Vitamin E-deficient jejuna were less responsive to exogenous noradrenaline, resulting in a smaller alpha 2-adrenergic-mediated decrease in intestinal short-circuit current. 8. Fasting for 72h produced a greater increment in intestinal short-circuit current in vitamin E-deficient jejuna. 9. Chronic vitamin E deficiency is prosecretory in the small intestine and may predispose to the perpetuation of protracted diarrhoeal diseases.

Absorption↗