Intestinal phenotypes in pediatric gallbladder epithelium

2011 ◽  
Vol 42 (10) ◽  
pp. 1454-1458 ◽  
Author(s):  
Yoh Zen ◽  
Chikako Zen ◽  
Alberto Quaglia ◽  
Mark Davenport ◽  
Nigel Heaton ◽  
...  
Author(s):  
G. I. Kaye ◽  
J. D. Cole

For a number of years we have used an adaptation of Komnick's KSb(OH)6-OsO4 fixation method for the localization of sodium in tissues in order to study transporting epithelia under a number of different conditions. We have shown that in actively transporting rabbit gallbladder epithelium, large quantities of NaSb(OH)6 precipitate are found in the distended intercellular compartment, while localization of precipitate is confined to the inner side of the lateral plasma membrane in inactive gallbladder epithelium. A similar pattern of distribution of precipitate has been demonstrated in human and rabbit colon in active and inactive states and in the inactive colonic epithelium of hibernating frogs.


2001 ◽  
Vol 120 (5) ◽  
pp. A386-A386 ◽  
Author(s):  
S NARINS ◽  
E PARK ◽  
X SU ◽  
P SMITH ◽  
M ABEDIN

2001 ◽  
Vol 120 (5) ◽  
pp. A386-A386
Author(s):  
S NARINS ◽  
J DOUGHERTY ◽  
E PARK ◽  
R NICHOLS ◽  
P SMITH ◽  
...  

1992 ◽  
Vol 99 (2) ◽  
pp. 241-262 ◽  
Author(s):  
G A Altenberg ◽  
J S Stoddard ◽  
L Reuss

In Necturus gallbladder epithelium, lowering serosal [Na+] ([Na+]s) reversibly hyperpolarized the basolateral cell membrane voltage (Vcs) and reduced the fractional resistance of the apical membrane (fRa). Previous results have suggested that there is no sizable basolateral Na+ conductance and that there are apical Ca(2+)-activated K+ channels. Here, we studied the mechanisms of the electrophysiological effects of lowering [Na+]s, in particular the possibility that an elevation in intracellular free [Ca2+] hyperpolarizes Vcs by increasing gK+. When [Na+]s was reduced from 100.5 to 10.5 mM (tetramethylammonium substitution), Vcs hyperpolarized from -68 +/- 2 to a peak value of -82 +/- 2 mV (P less than 0.001), and fRa decreased from 0.84 +/- 0.02 to 0.62 +/- 0.02 (P less than 0.001). Addition of 5 mM tetraethylammonium (TEA+) to the mucosal solution reduced both the hyperpolarization of Vcs and the change in fRa, whereas serosal addition of TEA+ had no effect. Ouabain (10(-4) M, serosal side) produced a small depolarization of Vcs and reduced the hyperpolarization upon lowering [Na+]s, without affecting the decrease in fRa. The effects of mucosal TEA+ and serosal ouabain were additive. Neither amiloride (10(-5) or 10(-3) M) nor tetrodotoxin (10(-6) M) had any effects on Vcs or fRa or on their responses to lowering [Na+]s, suggesting that basolateral Na+ channels do not contribute to the control membrane voltage or to the hyperpolarization upon lowering [Na+]s. The basolateral membrane depolarization upon elevating [K+]s was increased transiently during the hyperpolarization of Vcs upon lowering [Na+]s. Since cable analysis experiments show that basolateral membrane resistance increased, a decrease in basolateral Cl- conductance (gCl-) is the main cause of the increased K+ selectivity. Lowering [Na+]s increases intracellular free [Ca2+], which may be responsible for the increase in the apical membrane TEA(+)-sensitive gK+. We conclude that the decrease in fRa by lowering [Na+]s is mainly caused by an increase in intracellular free [Ca2+], which activates TEA(+)-sensitive maxi K+ channels at the apical membrane and decreases apical membrane resistance. The hyperpolarization of Vcs is due to increase in: (a) apical membrane gK+, (b) the contribution of the Na+ pump to Vcs, (c) basolateral membrane K+ selectivity (decreased gCl-), and (d) intraepithelial current flow brought about by a paracellular diffusion potential.


2014 ◽  
Vol 66 (3) ◽  
pp. 641-647
Author(s):  
F.S. Dias ◽  
I.F. Santos ◽  
R.M. Franco ◽  
E.R. Nascimento

Pathogenic microorganisms can reside transiently or permanently in the gallbladder of cattle. Thus, during slaughter, more attention should be given to the gastrointestinal tract, especially to the accessory organ, the gallbladder. The main aim of this study was to characterize the bacterial microbiota present in bile and gallbladder epithelium of cattle slaughtered in a slaughtering plant under sanitary conditions and to evaluate the antimicrobial resistance in strains of the genus Staphylococcus. Thirty intact gallbladders were collected and the in bile and epithelium were researched for the presence of Aerobic Mesophilic Heterotrophic Bacteria (AMHB), Staphylococcusspp., total Enterobacteriaceae, Enterococcus spp. and Salmonella spp. The frequency of isolation of the microorganism mentioned above were, respectively: 23.02%, 14.39%, 13.67%, 24.46%, 0% and 24.46%. Concerning both gallbladder environments, the frequency of isolation of the microorganisms in the epithelium was 64.03%, and in the bile 35.97%, with no statistical difference, but with significant difference between the population averages. In antimicrobial susceptibility testing, strains of Staphylococcusfrom both bile and gallbladder epithelium showed sensitivity to the antimicrobials: penicillin G, ceftriaxone, chloramphenicol and gentamicin. The observation that the gallbladder supports a high frequency of microorganisms brings us to the possible fact that cattle might be a persistent carrier of pathogens of great importance to public health.


1990 ◽  
Vol 259 (1) ◽  
pp. C56-C68 ◽  
Author(s):  
Y. Segal ◽  
L. Reuss

The apical membrane of Necturus gallbladder epithelium contains a voltage-activated K+ conductance [Ga(V)]. Large-conductance (maxi) K+ channels underlie Ga(V) and account for 17% of the membrane conductance (Ga) under control conditions. We examined the Ba2+, tetraethylammonium (TEA+), and quinine sensitivities of Ga and single maxi K+ channels. Mucosal Ba2+ addition decreased resting Ga in a concentration-dependent manner (65% block at 5 mM) and decreased Ga(V) in a concentration- and voltage-dependent manner. Mucosal TEA+ addition also decreased control Ga (60% reduction at 5 mM). TEA+ block of Ga(V) was more potent and less voltage dependent that Ba2+ block. Maxi K+ channels were blocked by external Ba2+ at millimolar levels and by external TEA+ at submillimolar levels. At 0.3 mM, quinine (mucosal addition) hyperpolarized the cell membranes by 6 mV and reduced the fractional apical membrane resistance by 50%, suggesting activation of an apical membrane K+ conductance. At 1 mM, quinine both activated and blocked K(+)-conductive pathways. Quinine blocked maxi K+ channel currents at submillimolar concentrations. We conclude that 1) Ba2+ and TEA+ block maxi K+ channels and other K+ channels underlying resting Ga; 2) parallels between the Ba2+ and TEA+ sensitivities of Ga(V) and maxi K+ channels support a role for these channels in Ga(V); and 3) quinine has multiple effects on K(+)-conductive pathways in gallbladder epithelium, which are only partially explained by block of apical membrane maxi K+ channels.


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