Diquat-Induced Intestinal Secretion in the Anaesthetized Rat

1992 ◽  
Vol 11 (6) ◽  
pp. 524-529 ◽  
Author(s):  
John M. Rawlings ◽  
John R. Foster ◽  
Jon R. Heylings
Keyword(s):  
Structural Damage ◽  
Fluid Transport ◽  
Mammalian Species ◽  
Intestinal Secretion ◽  
Fluid Secretion ◽  
Transport Processes ◽  
Secretory Response ◽  
Anaesthetized Rats ◽  
Anaesthetized Rat

1 Diquat (1,1'-ethylene-2,2'-bipyridilium) is a non-selective desiccant herbicide which, when administered orally to mammalian species, causes significant secretion of fluid into the lumen of the gastrointestinal tract. In order to characterize this secretory response in more detail the effect of sublethal doses of diquat dibromide (DQBr2) on intestinal secretion was investigated in vivo in the jejunum of anaesthetized rats. 2 Ligated segments of jejunum (10 cm) which were prepared in groups of up to five animals were filled with 500 μl of isosmotic DQBr2 solutions with concentrations ranging from 1-100 mM and maintained in the anaesthetized rat for 1, 2 or 3 h; in control experiments a solution of 100 mM NaBr was used. 3 It was found that while all of the fluid instilled into the segments was absorbed in the control experiments, there was both a dose- and time-dependent secretory response to DQBr2. Maximal fluid secretion occurred after treatment with 50 mM DQBr2 for 3 h. 4 Histological assessment of the jejunum revealed an increase in cell exfoliation and evidence of luminal distension after incubation with DQBr2. However, no structural damage to the mucosa could be seen to account for the fluid secretion. 5 The model described provides a quantitative means of evaluating intestinal secretion and may be used for elucidating the mechanism by which diquat alters fluid transport processes.

In vivo effect of volume expansion on rectal gland function. II. Hemodynamic changes

1984 ◽  
Vol 246 (1) ◽  
pp. R67-R71
Author(s):  
R. J. Solomon ◽  
M. Taylor ◽  
R. Rosa ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Blood Flow ◽  
Volume Expansion ◽  
Energy Requirement ◽  
Fluid Secretion ◽  
Chloride Secretion ◽  
Secretory Response ◽  
Rectal Gland ◽  
Oxygen Extraction Ratio ◽  
Humoral Factors

Intravascular volume expansion causes a 300% increase in the rate of fluid secretion from, and blood flow to, the in vivo rectal gland of the spiny dogfish Squalus acanthias. Similar increases are also observed in explanted rectal glands perfused through a catheter from the dorsal aorta of a volume-expanded dogfish. Stimulation of rectal gland secretion by volume expansion is not associated with a change in the ratio of chloride secreted to oxygen consumed by the rectal gland and the oxygen extraction ratio, suggesting that an increase in blood flow is necessary to support the increased rate of chloride secretion. Perfusion of the explanted gland with bumetanide (10(-4) M) completely inhibits the secretory response to volume expansion but does not prevent the increase in blood flow. Bumetanide also inhibits dibutyryl adenosine 3',5'-cyclic monophosphate- and theophylline-induced increases in chloride secretion but does not inhibit the hyperemic response. Somatostatin inhibits the secretory response of the explanted gland to volume expansion but does not prevent the increase in blood flow. Although an increase in blood flow is necessary to support the increased energy requirement of enhanced transport, the secretory response and the increase in blood flow appear to be independently regulated and mediated, at least in part, by humoral factors.

P2 purinoceptors regulate calcium-activated chloride and fluid transport in 31EG4 mammary epithelia

2003 ◽  
Vol 284 (4) ◽  
pp. C897-C909 ◽  
Author(s):  
Sasha Blaug ◽  
Jodi Rymer ◽  
Stephen Jalickee ◽  
Sheldon S. Miller
Keyword(s):  
Membrane Potential ◽  
Fluid Transport ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Fluid Secretion ◽  
Extracellular Nucleotides ◽  
Basolateral Membranes ◽  
Apical Side ◽  
Mammary Epithelia

It has been reported that secretory mammary epithelial cells (MEC) release ATP, UTP, and UDP upon mechanical stimulation. Here we examined the physiological changes caused by ATP/UTP in nontransformed, clonal mouse mammary epithelia (31EG4 cells). In control conditions, transepithelial potential (apical side negative) and resistance were −4.4 ± 1.3 mV (mean ± SD, n = 12) and 517.7 ± 39.4 Ω · cm2, respectively. The apical membrane potential was −43.9 ± 1.7 mV, and the ratio of apical to basolateral membrane resistance ( R A/ R B) was 3.5 ± 0.2. Addition of ATP or UTP to the apical or basolateral membranes caused large voltage and resistance changes with an EC50 of ∼24 μM (apical) and ∼30 μM (basal). Apical ATP/UTP (100 μM) depolarized apical membrane potential by 17.6 ± 0.8 mV ( n = 7) and decreased R A/ R B by a factor of ≈3. The addition of adenosine to either side (100 μM) had no effect on any of these parameters. The ATP/UTP responses were partially inhibited by DIDS and suramin and mediated by a transient increase in free intracellular Ca2+ concentration (427 ± 206 nM; 15–25 μM ATP, apical; n = 6). This Ca2+ increase was blocked by cyclopiazonic acid, by BAPTA, or by xestospongin C. 31EG4 MEC monolayers also secreted or absorbed fluid in the resting state, and ATP or UTP increased fluid secretion by 5.6 ± 3 μl · cm−2 · h−1( n = 10). Pharmacology experiments indicate that 31EG4 epithelia contain P2Y2 purinoceptors on the apical and basolateral membranes, which upon activation stimulate apical Ca2+-dependent Cl channels and cause fluid secretion across the monolayer. This suggests that extracellular nucleotides could play a fundamental role in mammary gland paracrine signaling and the regulation of milk composition in vivo.

Vagal control of fluid transport, transmural potential difference, and motility in the ferret jejunum

1985 ◽  
Vol 249 (6) ◽  
pp. G651-G654 ◽  
Author(s):  
B. Greenwood ◽  
N. W. Read
Keyword(s):  
Fluid Transport ◽  
Vagal Stimulation ◽  
Contractile Activity ◽  
Intestinal Transport ◽  
Intestinal Secretion ◽  
Potential Difference ◽  
Intraluminal Pressure ◽  
Jejunal Loop

The role of the vagus nerve in the control of intestinal transport was investigated in the ferret jejunum in vivo. Fluid transport was measured in an isolated 10-cm segment of jejunum by means of a single-pass perfusion technique with radioactive markers introduced into the perfusion fluid and the bloodstream of the animal. Transmural potential difference (PD) and intraluminal pressure in the perfused jejunal loop were also monitored. Vagal stimulation (20 Hz, 20 V, and 0.5 ms for 1 min) resulted in jejunal fluid movement in the direction of secretion, a rise in transmural PD, and an increase in jejunal contractile activity. Similar changes were induced by close intra-arterial injection of acetylcholine (20 micrograms X kg-1). The contractile response to vagal stimulation was abolished by atropine. Moreover, atropine did not block the changes in fluid transport and transmural PD that were induced by vagal stimulation, although the transmural PD response was reduced. The results suggest that vagal stimulation induces intestinal secretion accompanied by a rise in transmural PD; the events are mediated at least in part by a noncholinergic transmitter as yet undetermined.

Cholera toxin induces intestinal secretion in an acute renal failure rat model

2021 ◽  
Vol 01 ◽  
Author(s):  
Parvin Abraham ◽  
Anu Joseph ◽  
Parvathy Sreekumar ◽  
Koyikkal Karthikeya Varma ◽  
Lilly Madhavan
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Cholera Toxin ◽  
Diarrheal Disease ◽  
Intestinal Secretion ◽  
Fluid Secretion ◽  
Secretory Response ◽  
Histopathological Analysis ◽  
Intestinal Loop ◽  
Life Threatening

Background: Cholera is a life-threatening secretory diarrheal disease caused by Vibrio cholera bacterium. On the contrary, local and specific use of cholera toxin (CT) at a low concentration can cause controlled fluid secretion. In the study, we explored the secretory action of CT in the intestine of rats with acute renal failure (ARF). Methods: Closed intestinal loop experiments were performed in ARF rats treated with CT. Secreted fluid and serum were analyzed for various ¬solutes and electrolytes. The presence of K+, Na+, Cl-, urea and creatinine were monitored. Histopathology analysis was carried out to evaluate the effect of CT in liver, kidney, and intestinal tissues. Results: A reduction in the absorption of water and electrolytes was observed over time and a secretory response started to appear within hours of CT treatment. The fluid secretory response with entrapped electrolytes was profound in ARF rats. Histopathological analysis of CT exposed tissues revealed that apart from the tissue damage produced by acute renal failure, no CT induced cellular changes occurred. Conclusion: CT can be used as a secretagogue to induce fluid and electrolyte secretion in ARF rats. However, effective measures should be taken to avoid CT induced acidosis.

Effects of Tropisetron, a 5-Hydroxytryptamine Type 3 Receptor Blocker, on Intestinal Secretion Induced by Cholera Toxin or Deoxycholic Acid in Rabbits In Vivo

1993 ◽  
Vol 21 (6) ◽  
pp. 323-333 ◽  
Author(s):  
P K Bardhan ◽  
A S MH Rahman ◽  
S Islam ◽  
M Rahman ◽  
K Gyr
Keyword(s):  
Cholera Toxin ◽  
Deoxycholic Acid ◽  
Intraperitoneal Administration ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Intestinal Secretion ◽  
Fluid Secretion ◽  
Receptor Blocker ◽  
Type 3

It has been suggested that 5-hydroxytryptamine is involved in the pathogenesis of various intestinal hypersecretory states including cholera. In this study, the effect of tropisetron (ICS 205-930), a specific 5-hydroxytryptamine type-3 receptor blocker, on jejunal and colonic fluid secretion induced respectively by cholera toxin and deoxycholic acid was investigated in rabbits using isolated loops of intestine in vivo. Marked fluid accumulation in both the jejunal and colonic loops was observed after exposure to cholera toxin and deoxycholic acid respectively. Elevation of jejunal and colonic mucosal cyclic adenosine monophosphate concentrations was also noted. Intraperitoneal administration of tropisetron dose-dependent inhibited jejunal secretion induced by cholera toxin. In contrast, no significant anti-secretory effect of tropisetron was observed against colonic secretion induced by deoxycholic acid. Tropisetron did not affect elevated mucosal cyclic adenosine monophosphate concentrations. The inhibitory effect of tropisetron on intestinal secretion induced by cholera toxin, which was independent of cyclic adenosine monophosphate formation, suggests that 5- hydroxytryptamine plays an important role in this type of secretion.

Cultured human nasal epithelial multicellular spheroids: polar cyst-like model tissues

1991 ◽  
Vol 69 (2-3) ◽  
pp. 102-108 ◽  
Author(s):  
Michael A. Bridges ◽  
David C. Walker ◽  
Robert A. Harris ◽  
Bruce R. Wilson ◽  
A. George F. Davidson
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Fluid Transport ◽  
Airway Epithelial Cells ◽  
Transport Processes ◽  
Epithelial Tissue ◽  
Airway Epithelial ◽  
Multicellular Spheroids ◽  
Human Respiratory Tract

We report here a new readily cultured nonadherent hollow spheroidal epithelial tissue model: human nasal epithelial multicellular spheroids, prepared from brushings of human nasal epithelium in vivo. Although cultured cyst-like epithelial models developed from embryonic, transformed, or polypoid tissues have been reported previously, human nasal epithelial multicellular spheroids are derived from normal mature nontransformed human airway epithelial cells. In our studies, spheroids ranged in size from 50 to 700 μm diameter (averaging approximately 250 μm). Cells of the spheroid displayed morphological polarity and formed junctional complexes. Transcellular electrolyte transport may underlie the increase in spheroid size which occurred in culture. The ease and simplicity of the brushing and culture procedures reported here render normal and diseased human cell populations more readily accessible to investigation. We believe human nasal epithelial multicellular spheroids may have important applications in the study of electrolyte and fluid transport processes, ciliary motility, epithelial polarity, cellular metabolism, and drug cytotoxicity in normal and pathophysiological states of the human respiratory tract (e.g., cystic fibrosis).Key words: cultured airway epithelial cells, electrolyte and fluid transport, spheroid, cyst, cystic fibrosis.

cAMP-dependent exocytosis and vesicle traffic regulate CFTR and fluid transport in rat jejunum in vivo

2003 ◽  
Vol 284 (2) ◽  
pp. C429-C438 ◽  
Author(s):  
Nadia A. Ameen ◽  
Christopher Marino ◽  
Pedro J. I. Salas
Keyword(s):  
Fluid Transport ◽  
Fluid Secretion ◽  
Cell Types ◽  
Surface Proteins ◽  
Apical Surface ◽  
Rat Jejunum ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Vesicle Traffic

The cystic fibrosis transmembrane conductance regulator (CFTR) channel is regulated by cAMP-dependent vesicle traffic and exocytosis to the apical membrane in some cell types, but this has not been demonstrated in the intestinal crypt. The distribution of CFTR, lactase (control), and fluid secretion were determined in rat jejunum after cAMP activation in the presence of nocodazole and primaquine to disrupt vesicle traffic. CFTR and lactase were localized by immunofluorescence, and surface proteins were detected by biotinylation of enterocytes. Immunoprecipitates from biotinylated and nonbiotinylated cells were analyzed by streptavidin detection and immunoblots. Immunolocalization confirmed a cAMP-dependent shift of CFTR but not lactase from a subapical compartment to the apical surface associated with fluid secretion that was reduced in the presence of primaquine and nocodazole. Analysis of immunoblots from immunoprecipitates after biotinylation revealed a 3.8 ± 1.7-fold ( P < 0.005) increase of surface-exposed CFTR after vasoactive intestinal peptide (VIP). These measurements provide independent corroboration supporting a role for vesicle traffic in regulating CFTR and cAMP-induced fluid transport in the intestine.

Mechanism of production of intestinal secretion by negative luminal pressure.

1977 ◽  
Vol 233 (5) ◽  
pp. E416
Author(s):  
A A Hakim ◽  
C B Papeleux ◽  
J B Lane ◽  
N Lifson ◽  
M E Yablonski
Keyword(s):  
Plasma Concentration ◽  
Hydrostatic Pressure ◽  
Fluid Transport ◽  
Venous Pressure ◽  
Strong Support ◽  
Intestinal Secretion ◽  
Fluid Transfer

The relationships between luminal hydrostatic pressure and fluid transport by dog jejunum in vivo studied as a sheet in the Wells clamp were compared with quantitative predictions from a model proposed for the mechanism of the secretion produced by elevated venous pressure. According to the model, the secretion produced by increasing venous pressure and the secretion produced by negative luminal pressure are both passive filtrates contingent on a transepithelial pressure of a few centimeters of H2O. We consider that the agreement between the observed and predicted responses to luminal pressure provides strong support for the model. In particular, a) the observations displayed a predicted gross asymmetry in rates of fluid transfer with isotonic fluids depending on whether the luminal pressure was positive or negative; b) the observed magnitude of the negative luminal pressure required for the onset of secretion agreed with predictions; and c) the secretion contained significant amounts of protein at about 25% of the plasma concentration.

Pseudomonas aeruginosainduces changes in fluid transport across airway surface epithelia

1998 ◽  
Vol 275 (5) ◽  
pp. C1284-C1290 ◽  
Author(s):  
D. J. Evans ◽  
P. S. Matsumoto ◽  
J. H. Widdicombe ◽  
C. Li-Yun ◽  
A. A. Maminishkis ◽  
...  
Keyword(s):  
Fluid Transport ◽  
Bacterial Colonization ◽  
Organic Anion ◽  
Ionic Composition ◽  
Basolateral Membrane ◽  
Fluid Secretion ◽  
Fluid Absorption ◽  
Gene Encoding ◽  
Transport Inhibitors

Fluid transport across cultures of bovine tracheal epithelium was measured with a capacitance probe technique. Baseline fluid absorption ( Jv) across bovine cells of 3.2 μl ⋅ cm−2⋅ h−1was inhibited by ∼78% after 1 h of exposure to suspensions of Pseudomonas aeruginosa, with a concomitant decrease in transepithelial potential (TEP) and increase in transepithelial resistance ( Rt). Effects of P. aeruginosa were blocked by amiloride, which decreased Jvby 112% from baseline of 2.35 ± 1.25 μl ⋅ cm−2⋅ h−1, increased Rtby 101% from baseline of 610 ± 257 Ω ⋅ cm2, and decreased TEP by 91% from baseline of −55 ± 18.5 mV. Microelectrode studies suggested that effects of P. aeruginosa on amiloride-sensitive Na absorption were due in part to a block of basolateral membrane K channels. In the presence of Cl transport inhibitors [5-nitro-2-(3-phenylpropylamino)-benzoic acid, H2-DIDS, and bumetanide], P. aeruginosa induced a fluid secretion of ∼2.5 ± 0.4 μl ⋅ cm−2⋅ h−1and decreased Rtwithout changing TEP. However, these changes were abolished when the transport inhibitors were used in a medium in which Cl was replaced by an impermeant organic anion. Filtrates of P. aeruginosa suspensions had no effect on Jv, TEP, or Rt. Mutants lacking exotoxin A or rhamnolipids or with defective lipopolysaccharide still inhibited fluid absorption and altered bioelectrical properties. By contrast, mutations in the rpoN gene encoding a ς factor of RNA polymerase abolished actions of P. aeruginosa. In vivo, changes in transepithelial salt and water transport induced by P. aeruginosa may alter viscosity and ionic composition of airway secretions so as to foster further bacterial colonization.

scholarly journals Novel Role for Albumin in Innate Immunity: Serum Albumin Inhibits the Growth of Blastomyces dermatitidis Yeast Form In Vitro

2003 ◽  
Vol 71 (11) ◽  
pp. 6648-6652 ◽  
Author(s):  
Steven Giles ◽  
Charles Czuprynski
Keyword(s):  
Molecular Weight ◽  
Inhibitory Activity ◽  
Mammalian Species ◽  
Blastomyces Dermatitidis ◽  
Low Molecular Weight ◽  
Rat Serum ◽  
Yeast Form ◽  
Domain Iii

ABSTRACT In this study we found that serum inhibitory activity against Blastomyces dermatitidis was principally mediated by albumin. This was confirmed in experiments using albumin from several mammalian species. Analbuminemic rat serum did not inhibit B. dermatitidis growth in vivo; however, the addition of albumin restored inhibitory activity. Inhibitory activity does not require albumin domain III and appears to involve binding of a low-molecular-weight yeast-derived growth factor.

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