Rectal Mucosal Histamine Release in Ulcerative Colitis

1980 ◽  
Vol 59 (5) ◽  
pp. 389-391 ◽  
Author(s):  
D. S. Rampton ◽  
R. D. Murdoch ◽  
G. E. Sladen
Keyword(s):  
Ulcerative Colitis ◽  
Histamine Release ◽  
Electrical Potential ◽  
Electrical Potential Difference ◽  
Hypersensitivity Reactions ◽  
Epithelial Permeability ◽  
Immediate Hypersensitivity ◽  
Histamine Production ◽  
Active Colitis

1. Rectal dialysis in vivo was used to assess rectal mucosal release of histamine in patients with ulcerative colitis and in control subjects. 2. Rectal mucosal histamine release was significantly increased in ulcerative colitis, whether the patients were in remission or relapse. The highest values were found in active colitis, but in several such patients histamine release was within the control range. Measurement of rectal mucosal electrical potential difference suggested that increased mucosal histamine release in this group of patients was not due to enhanced epithelial permeability. 3. Rectal dialysis appears to be a useful method for assessing mucosal histamine production and the results obtained are consistent with the hypothesis that immediate hypersensitivity reactions could be of importance in some patients with ulcerative colitis.

Active electrolyte transport in mammalian buccal mucosa

1988 ◽  
Vol 255 (3) ◽  
pp. G286-G291 ◽  
Author(s):  
R. C. Orlando ◽  
N. A. Tobey ◽  
V. J. Schreiner ◽  
R. D. Readling
Keyword(s):  
Buccal Mucosa ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrolyte Transport ◽  
Electrical Potential Difference ◽  
Ussing Chambers ◽  
Net Fluxes

The transmural electrical potential difference (PD) was measured in vivo across the buccal mucosa of humans and experimental animals. Mean PD was -31 +/- 2 mV in humans, -34 +/- 2 mV in dogs, -39 +/- 2 mV in rabbits, and -18 +/- 1 mV in hamsters. The mechanisms responsible for this PD were explored in Ussing chambers using dog buccal mucosa. After equilibration, mean PD was -16 +/- 2 mV, short-circuit current (Isc) was 15 +/- 1 microA/cm2, and resistance was 1,090 +/- 100 omega.cm2, the latter indicating an electrically "tight" tissue. Fluxes of [14C]mannitol, a marker of paracellular permeability, varied directly with tissue conductance. The net fluxes of 22Na and 36Cl were +0.21 +/- 0.05 and -0.04 +/- 0.02 mueq/h.cm2, respectively, but only the Na+ flux differed significantly from zero. Isc was reduced by luminal amiloride, serosal ouabain, or by reducing luminal Na+ below 20 mM. This indicated that the Isc was determined primarily by active Na+ absorption and that Na+ traverses the apical membrane at least partly through amiloride-sensitive channels and exits across the basolateral membrane through Na+-K+-ATPase activity. We conclude that buccal mucosa is capable of active electrolyte transport and that this capacity contributes to generation of the buccal PD in vivo.

scholarly journals Transmural electrical potential difference in the mammalian esophagus in vivo

1978 ◽  
Vol 75 (2) ◽  
pp. 286-291 ◽  
Author(s):  
Keith S. Turner ◽  
Don W. Powell ◽  
Charles N. Carney ◽  
Roy C. Orlando ◽  
Eugene M. Bozymski
Keyword(s):  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference

Lung volumes after antigen infusion in the guinea pig in vivo: effects of vagal section

1978 ◽  
Vol 45 (6) ◽  
pp. 957-961 ◽  
Author(s):  
J. M. Drazen ◽  
S. H. Loring ◽  
C. Venugopalan
Keyword(s):  
Total Lung Capacity ◽  
Hypersensitivity Reactions ◽  
Immediate Hypersensitivity ◽  
Similar Extent ◽  
Static Compliance ◽  
Lung Volumes ◽  
Lung Capacity ◽  
In Vivo Effects ◽  
Gas Volume

The effects of intravenous antigen infusion on lung volumes and quasi-static deflationary pulmonary compliance in guinea pigs previously sensitized to ovalbumin were studied in vivo. Ovalbumin infusion significantly increased minimal gas volume to a similar extent in animals with intact or cut vagi. Total lung capacity fell only in animals with intact vagi. Quasi-static compliance fell in both groups of animals, but the fall was significantly greater in animals with intact vagi. These data demonstrate that immediate hypersensitivity reactions alter lung volumes and the elastic properties of the lung by both vagal dependent and vagal independent mechanisms.

In Vivo Cysteinyl Leukotriene Release in Allergic and Nonallergic Immediate Hypersensitivity Reactions during Anesthesia

2017 ◽  
Vol 126 (5) ◽  
pp. 834-841 ◽  
Author(s):  
Dominique Laroche ◽  
Pierre Léturgie ◽  
Delphine Mariotte ◽  
Yann Ollivier ◽  
Jean-Luc Hanouz ◽  
...  
Keyword(s):  
Mast Cell ◽  
Skin Tests ◽  
Hypersensitivity Reactions ◽  
Immediate Hypersensitivity ◽  
Mast Cell Tryptase ◽  
Cysteinyl Leukotriene ◽  
Negative Results ◽  
Important Mediator ◽  
The Difference

Abstract Background Immediate hypersensitivity reactions occurring during anesthesia are classified as allergic when skin tests and mast cell tryptase are positive and as nonallergic when negative results are obtained. Cysteinyl leukotrienes (cysLTs) are potent mediators synthesized by mast cell and eosinophil that induce bronchial constriction. They could play a role in hypersensitivity reactions. Methods cysLT C4, D4, and E4 concentrations were measured by a competition immunoassay in serial plasma samples obtained prospectively from 21 anesthetized controls and retrospectively from 34 patients who reacted at induction of anesthesia (24 with allergic and 10 with nonallergic reactions). Results In controls, the median (interquartile range) cysLT concentration was 0.83 (0.69 to 1.02) μg/l before anesthesia and was unchanged 30 min, 6 h, and 24 h afterward. In the patients with allergic reactions, the values were highly increased 30 to 60 min after the reaction (17.9 [7.8 to 36.0] μg/l), while the patients with nonallergic reactions had less increased values (7.3 [3.0 to 11.5] μg/l). The difference between the three groups was significant (P < 0.0001). Increased values persisted during the 24 h of observation. Concentrations were significantly higher in patients with bronchospasm (P = 0.016). Conclusions cysLTs appear to be an important mediator of allergic and nonallergic immediate hypersensitivity reactions. These findings might open a new field for management of patients with hypersensitivity reactions, especially nonallergic ones.

Sodium transport and the cellular sodium transport pool of colonic epithelium: effects of sodium loading, aldosterone and lithium

1987 ◽  
Vol 112 (2) ◽  
pp. 247-252 ◽  
Author(s):  
C. J. Edmonds ◽  
J. Mackenzie
Keyword(s):  
Epithelial Cells ◽  
Sodium Transport ◽  
Time Course ◽  
Electrical Potential ◽  
Electrical Potential Difference ◽  
Active Sodium ◽  
Prolonged Infusion ◽  
Sodium Loading ◽  
Sodium Flux

ABSTRACT The cellular sodium transport pool and sodium transepithelial fluxes were investigated in vivo in rat distal colon in relation to sodium loading by intravenous infusion (3·5 h), and to short (4 h) and prolonged (72 h) i.v. administration of aldosterone. Considerable natriuresis and increase in body sodium content were produced by the sodium load but there was no significant effect on the transcellular sodium flux (active absorption from lumen to plasma) or on the sodium transport pool. Both short and prolonged aldosteronism produced similar increases in the transport pool and in the transcellular sodium flux, but the transepithelial electrical potential difference (p.d.) was significantly greater in rats given the prolonged infusion. Addition of amiloride to the solution in the lumen of the colon almost completely abolished the p.d., the transport pool and the transcellular sodium flux of the rats receiving prolonged infusion, but had much less effect in those given the short infusion. The time-course of recovery of p.d. following prolonged aldosteronism was similar to that described for the turnover rate of rat colonic epithelial cells. Lithium within the lumen had no significant effect in untreated rats but after prolonged aldosterone infusion lithium reduced the p.d. and the transcellular sodium flux although the transport pool was not reduced. These findings are consistent with the hypothesis that aldosteronism renders the apical membranes of the epithelial cells permeable to lithium and that intracellular accumulation of lithium depresses active sodium transfer. The observations are interpreted in terms of an epithelial model in which aldosterone induces amiloride-sensitive pathways (diffusion channels permeable to sodium and lithium) in the apical membrane which totally replace the amiloride-insensitive pathways when aldosteronism is prolonged; the resulting expansion of the sodium transport pool is the stimulus for increased active sodium transport across the basolateral membranes. J. Endocr. (1987) 112, 247–252

An Investigation of the Role of Possible Neural Mechanisms in Cholera Toxin-Induced Secretion in Rabbit Ileal Mucosa in Vitro

1989 ◽  
Vol 77 (2) ◽  
pp. 161-166 ◽  
Author(s):  
K. J. Moriarty ◽  
N. B. Higgs ◽  
M. Woodford ◽  
L. A. Turnberg
Keyword(s):  
Cholera Toxin ◽  
Fluid Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Rabbit Ileum ◽  
Ileal Mucosa

1. Cholera toxin stimulates intestinal secretion in vitro by activation of mucosal adenylate cyclase. However, it has been proposed that cholera toxin promotes secretion in vivo mainly through an indirect mechanism involving enteric neural reflexes. 2. We examined this hypothesis further by studying the influence of neuronal blockade on cholera toxin-induced changes in fluid transport across rabbit ileum in vitro. Mucosa, stripped of muscle layers, was mounted in flux chambers and luminal application of crude cholera toxin (2 μg/ml) caused a delayed but sustained rise in the short-circuit current, electrical potential difference and Cl− secretion. Pretreatment with the nerve-blocking drug, tetrodotoxin (5 × 10−6 mol/l serosal side), failed to influence the secretory response to cholera toxin, and addition of tetrodotoxin at the peak response to cholera toxin also had no effect. 3. That tetrodotoxin could block neurally mediated secretagogues was confirmed by the demonstration that the electrical responses to neurotensin (10−7 mol/l and 10−8 mol/l) were blocked by tetrodotoxin (5 × 10−6 mol/l). Furthermore, the response to cholera toxin of segments of ileum, which included the myenteric, submucosal and mucosal nerve plexuses, was not inhibited by tetrodotoxin. 4. We conclude that cholera toxin-induced secretion in rabbit ileum in vitro is not mediated via a neurological mechanism.

scholarly journals Effects of cholecalciferol on the translocation of calcium by non-everted ileum in vitro

1975 ◽  
Vol 152 (2) ◽  
pp. 181-190 ◽  
Author(s):  
Eric S. Holdsworth ◽  
John E. Jordan ◽  
Ellen Keenan
Keyword(s):  
Sodium Dodecyl ◽  
Electrical Potential ◽  
Basement Membranes ◽  
Metabolic Energy ◽  
Temperature Sensitive ◽  
Mucosal Cell ◽  
Electrical Potential Difference ◽  
Mucosal Cells

An apparatus is described that allows perfusion of a non-everted segment of intestine in vitro and the study of the accumulation of substances within the mucosal cells. The translocation of Ca2+ by rachitic-chick ileum and the effect of pretreatment with cholecalciferol was investigated, with the following conclusions. (1) Entry of Ca2+ across the microvilli into mucosal cells is by diffusion; it does not require metabolic energy or the presence of any other inorganic ions. (2) Pretreatment of the chick with cholecalciferol causes increased permeability of the microvillus to Ca2+ in both directions (lumen to cell, cell to lumen). The increased transport brought about by cholecalciferol in vivo can be partially mimicked by sodium dodecyl sulphate added in vitro. (3) The sign and the magnitude of the electrical potential difference prevailing across the ileum does not influence Ca2+ transport. (4) Exit of Ca2+ from the mucosal cell is temperature-sensitive, requires metabolic energy and Na+. (5) Pretreatment with cholecalciferol caused increased movement of Ca2+ out of the cell across the basement membranes. This effect of cholecalciferol given in vivo could be markedly increased by the presence of dicyclohexylcarbodi-imide in the perfusion fluid. These observations suggested that cholecalciferol increased Ca2+ entry (and exit) at the mucosal surface and also caused Ca2+ to be more available to the pump at the serosal surface.

Sign in / Sign up

Export Citation Format

Share Document