Effect of heat stress on rabbit esophageal epithelium

1999 ◽  
Vol 276 (6) ◽  
pp. G1322-G1330 ◽  
Author(s):  
Nelia A. Tobey ◽  
Dipali Sikka ◽  
Esteban Marten ◽  
Canan Caymaz-Bor ◽  
S. Seraj Hosseini ◽  
...  

Hot beverages expose the esophageal epithelium to temperatures as high as 58°C. To study the impact of such temperatures, rabbit esophageal epithelium was exposed to luminal heat or both luminal and serosal heat while mounted in Ussing chambers. Luminal heat, mimicking exposure to hot beverages, reduced potential difference (PD) and resistance ( R) when applied at ≥49°C and reduced short-circuit current ( I sc) at ≥60°C. At ≥60°C, subepithelial blisters developed. Higher temperatures reduced R only moderately and reversibly. In contrast, the I sc declined sharply and irreversibly once threshold was reached. Luminal and serosal heat also reduced PD, I sc, and R, although the threshold for reduction in I scwas now similar to that for R. Additionally, luminal and serosal heat reduced I sc more than R for any given temperature and resulted in blisters at lower temperatures (50°C) than luminal heat alone. The heat-induced decline in I sc was attributed in part to inactivation of Na-K-ATPase activity, although other transport systems could have been equally affected, and the decline in R to an increase in paracellular permeability. The latter effect on R also contributed to an increase in tissue sensitivity to luminal acid damage. Consumption of hot beverages exposes the esophagus to temperatures that can negatively impact epithelial structure and function. Impaired barrier function by heat increases the risk of esophageal damage by subsequent contact with (refluxed) gastric acid. These findings help explain in part the association between esophageal disease and consumption of hot beverages.

2007 ◽  
Vol 292 (3) ◽  
pp. G796-G805 ◽  
Author(s):  
N. A. Tobey ◽  
C. M. Argote ◽  
M. S. Awayda ◽  
X. C. Vanegas ◽  
R. C. Orlando

Esophageal epithelial cells contain an apical cation channel that actively absorbs sodium ions (Na+). Since these channels are exposed in vivo to acid reflux, we sought the impact of high acidity on Na+channel function in Ussing-chambered rabbit epithelium. Serosal nystatin abolished short-circuit current ( Isc) and luminal pH titrated from pH 7.0 to pH ≥ 2.0 had no effect on Isc. Circuit analysis at pH 2.0 showed small, but significant, increases in apical and shunt resistances. At pH < 2.0, Iscincreased whereas resistance ( RT) decreased along with an increase in fluorescein flux. The change in Isc, but not RT, was reversible at pH 7.4. Reducing pH from 7.0 to 1.1 with H2SO4gave a similar pattern but higher Iscvalues, suggesting shunt permselectivity. A 10:1 Na+gradient after nystatin increased Iscby ∼4 μAmps/cm2and this declined at pH ≤ 3.5 until it reached ∼0.0 at pH 2.0. Impedance analysis on acid-exposed (non-nystatin treated) tissues showed compensatory changes in apical (increase) and basolateral (decrease) resistance at modest luminal acidity that were poorly reversible at pH 2.0 and associated with declines in capacitance, a reflection of lower apical membrane area. In esophageal epithelium apical cation channels transport Na+at gradients as low as 10:1 but do not transport H+at gradients of 100,000:1 (luminal pH 2.0). Luminal acid also inhibits Na+transport via the channels and abolishes it at pH 2.0. These effects on the channel may serve as a protective function for esophageal epithelium exposed to acid reflux.


1998 ◽  
Vol 274 (5) ◽  
pp. G819-G826 ◽  
Author(s):  
Serhat Bor ◽  
Canan Caymaz-Bor ◽  
Nelia A. Tobey ◽  
Solange Abdulnour-Nakhoul ◽  
Esteban Marten ◽  
...  

Epidemiological studies indicate a relationship between alcohol consumption and esophageal epithelial disease. We therefore sought the contribution of the direct effects of ethanol on esophageal epithelial structure and (transport and barrier) function. Epithelium from the rabbit was mounted in Ussing chambers and exposed luminally for 1 h to 1–40% ethanol. At concentrations of 1–5% potential difference (PD) increased, and at 10–40% PD decreased. The increase in PD with 1–5% ethanol was accompanied by an increase in short-circuit current ( Isc), and this increase in Isccould be blocked by ouabain pretreatment. The decrease in PD with 10–40% ethanol was associated with a decrease in electrical resistance ( R), and this decrease in R was paralleled by an increase in transepithelial [14C]mannitol flux. Reversibility of these changes was limited at ethanol concentrations ≥10%, and these were associated morphologically by patchy or diffuse tissue edema. Moreover, as with ethanol exposure in vitro, exposure in vivo produced dose-dependent changes in PD, Isc, R, and morphology. These observations indicate that exposure to ethanol in concentrations and under conditions reflecting alcohol consumption in humans can alter and impair esophageal epithelial transport and barrier functions. Such impairments are likely to contribute to the observed increase in risk of esophageal disease with regular consumption of alcoholic beverages.


2013 ◽  
Vol 448-453 ◽  
pp. 1732-1737
Author(s):  
Liu Bin ◽  
Hong Wei Cui ◽  
Li Xu ◽  
Kun Wang ◽  
Zhu Zhan ◽  
...  

This paper analyses the characteristics of large-scale offshore wind farm collection network and the impact of the medium voltage collection system optimization,while from the electrical technology point,it proposes the short circuit current of the collection network computational model and algorithms,based on the principle of equivalent circuit.Taking a wind power coolection system planned for a certain offshore wind farm planning for example, the validity of the model and algorithm is verified.


2004 ◽  
Vol 286 (5) ◽  
pp. G814-G821 ◽  
Author(s):  
Bi-Guang Tuo ◽  
Jimmy Y. C. Chow ◽  
Kim E. Barrett ◽  
Jon I. Isenberg

PKC has been shown to regulate epithelial Cl- secretion in a variety of models. However, the role of PKC in duodenal mucosal bicarbonate secretion is less clear. We aimed to investigate the role of PKC in regulation of duodenal mucosal bicarbonate secretion. Bicarbonate secretion by murine duodenal mucosa was examined in vitro in Ussing chambers using a pH-stat technique. PKC isoform expression and activity were assessed by Western blotting and in vitro kinase assays, respectively. PMA (an activator of PKC) alone had no effect on duodenal bicarbonate secretion or short-circuit current ( Isc). When PMA and dibutyryl-cAMP (db-cAMP) were added simultaneously, PMA failed to alter db-cAMP-stimulated duodenal bicarbonate secretion or Isc ( P > 0.05). However, a 1-h preincubation with PMA potentiated db-cAMP-stimulated duodenal bicarbonate secretion and Isc in a concentration-dependent manner (from 10-8 to 10-5M) ( P < 0.05). PMA preincubation had no effects on carbachol- or heat-stable toxin-stimulated bicarbonate secretion. Western blot analysis revealed that PKCα, -γ, -ϵ, -θ, -μ, and -ι/λ were expressed in murine duodenal mucosa. Ro 31–8220 (an inhibitor active against PKCϵ, -α, -β, and -γ), but not Gö 6983 (an inhibitor active against PKCα, -γ, -β, and -δ), reversed the potentiating effect of PMA on db-cAMP-stimulated bicarbonate secretion. PMA also time- and concentration-dependently increased the activity of PKCϵ, an effect that was prevented by Ro 31–8220 but not Gö 6983. These results demonstrate that activation of PKC potentiates cAMP-stimulated duodenal bicarbonate secretion, whereas it does not modify basal secretion. The effect of PKC on cAMP-stimulated bicarbonate secretion is mediated by the PKCϵ isoform.


1988 ◽  
Vol 255 (2) ◽  
pp. G247-G252 ◽  
Author(s):  
A. N. Charney ◽  
J. I. Scheide ◽  
P. M. Ingrassia ◽  
J. A. Zadunaisky

Chloride absorption in the small intestine of the winter flounder, Pseudopleuronectes americanus, is reported to be sensitive to ambient pH. We studied this sensitivity in isolated stripped intestinal mucosa mounted in modified Ussing chambers. Unidirectional 36Cl fluxes (JClm----s, JCls----m) were measured under short-circuited conditions in bathing solutions containing various combinations of HCO3- (0-20 mM), partial pressure of CO2 (0-36 mmHg), and pH (6.77-7.85). We found that JClm----s, net 36Cl flux (JClnet), and short-circuit current (Isc) increased and JCls----m decreased predominately in response to increases in bathing solution pH. There was a linear relationship between pH and both JClnet (r = 0.92, P less than 0.01) and Isc (r = 0.96, P less than 0.005) between pH 6.77 and 7.74. The pH effect was completely reversible, did not require either CO2 or HCO3-, and was not affected by the presence of mucosal barium at 1 mM. Mucosal bumetanide (0.1 mM) completely inhibited the pH effect. These data suggest that the process by which Cl- is absorbed in the flounder intestine is sensitive to pH. The data do not indicate whether pH affects Na+-K+-2Cl- cotransport or a Cl- transport pathway in series with this process. The direction of Cl- absorption in response to pH contrasts with inverse relation of pH and Cl- absorption in mammalian small intestine.


1988 ◽  
Vol 255 (3) ◽  
pp. G286-G291 ◽  
Author(s):  
R. C. Orlando ◽  
N. A. Tobey ◽  
V. J. Schreiner ◽  
R. D. Readling

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.


Author(s):  
Mandava Mohana Rao ◽  
Moutusi Paul ◽  
H.S. Jain

Fault-proof earthing switches are one of the important modules of a gas insulated substation, as it enables make at 100 percent short circuit current, which is functionally different from maintenance earthing switches. The fault-proof earthing switch shall be designed to make and break electro-magnetically and electro-statically induced currents as per IEC-62271-102. The paper discusses the impact of “test circuit configurations and voltage” on test parameters for gas insulated fault-proof earthing switch utilizing simulation with PSCAD software. Authors record the development of a 145 kV gas insulated fault proof earthing switch by considering novel design features like minimum arcing/pre-arcing time, effective current transfer from arcing contact to ground terminal, etc. The development has been evaluated successfully for electro-magnetically and electro-statically induced current duties as per IEC. Finally, design parameters to be considered for ensuring reliable performance during induced current switching from fault-proof earthing switches are also discussed.


1990 ◽  
Vol 259 (6) ◽  
pp. L459-L467 ◽  
Author(s):  
G. J. Tessier ◽  
T. R. Traynor ◽  
M. S. Kannan ◽  
S. M. O3'Grady

Equine tracheal epithelium, stripped of serosal muscle, mounted in Ussing chambers, and bathed in plasmalike Ringer solution generates a serosa-positive transepithelial potential of 10–22 mV and a short-circuit current (Isc) of 70–200 microA/cm2. Mucosal amiloride (10 microM) causes a 40–60% decrease in Isc and inhibits the net transepithelial Na flux by 95%. Substitution of Cl with gluconate resulted in a 30% decrease in basal Isc. Bicarbonate substitution with 20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid decreased the Isc by 21%. The Cl-dependent Isc was inhibited by serosal addition of 1 mM amiloride. Bicarbonate replacement or serosal amiloride (1 mM) inhibits the net Cl flux by 72 and 69%, respectively. Bicarbonate replacement significantly reduces the effects of serosal amiloride (1 mM) on Isc, indicating its effect is HCO3 dependent. Addition of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP; 100 microM) causes a 40% increase in Isc. This effect is inhibited by subsequent addition of 10 microM serosal bumetanide. Bumetanide (10 microM) reduces net Cl secretion following stimulation with 8-BrcAMP (100 microM). Serosal addition of BaCl2 (1 mM) causes a reduction in Isc equal to that following Cl replacement in the presence or absence of 100 microM cAMP. These results suggest that 1) Na absorption depends on amiloride-inhibitable Na channels in the apical membrane, 2) Cl influx across the basolateral membrane occurs by both a Na-H/Cl-HCO3 parallel exchange mechanism under basal conditions and by a bumetanide-sensitive Na-(K?)-Cl cotransport system under cAMP-stimulated conditions, and 3) basal and cAMP-stimulated Cl secretion depends on Ba-sensitive K channels in the basolateral membrane.


2002 ◽  
Vol 282 (6) ◽  
pp. G972-G980 ◽  
Author(s):  
Paula Miceli ◽  
Gerald P. Morris ◽  
Wallace K. MacNaughton ◽  
Stephen Vanner

The efferent secretomotor activity of capsaicin-sensitive nerves was monitored during the evolution of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced ileitis in the guinea pig by recording changes in short-circuit current (Δ I sc) in response to capsaicin, substance P (SP), and carbachol. Submucosal-mucosal preparations mounted in standard Ussing chambers were studied at time 0, at 8 h, and 1, 3, 5, 7, 14, and 30 days following the intraluminal instillation of TNBS or saline. Maximal Δ I scresponses to capsaicin were dramatically attenuated (54%) by 24 h. By day 7, SP- and TTX-insensitive carbachol-stimulated Δ I sc were also significantly reduced. Similar attenuation in capsaicin and carbachol responses was observed in jejunal tissue 20 cm proximal to the inflamed site at day 7. These studies demonstrate that efferent secretomotor function of capsaicin-sensitive nerves is maintained early in TNBS ileitis but significantly reduced by 24 h. By day 7, defects in enterocyte secretory function at inflamed and noninflamed sites also occurred, an effect that may be mediated by circulating cytokines.


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