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PubMed1994

[GFAP immunoreactivity in newly formed ileal mucosa in a serosal patch in dog colon].

A Short bowel was induced in 8 beagle bitches by resecting 85% of the small intestine. Following resection, a tangential fixation was performed in antiperistaltic direction between the ileum and the proximal colon. A 15 cm segment of the remaining ileum was incised opposite to its mesenterial attachment and sewn onto the serosa of the neighboring segment of colon (Serosa patching). After 20 weeks of observation, segments of the ileum, the colon and the anastomosed intestinal segment were removed. The neomucosa covering the patch surface was investigated using immunohistochemical methods in order to demonstrate the presence of nerve fibers. The immunofluorescence reaction using anti-GFAP (glial fibrillary acidic protein) clearly demonstrated immunoreactivity in the formed neomucosa and in the underlying granulation tissue. The immunoreactive fibers were comparable with fibers demonstrated in the original mucosa. This finding is an indication that the neomucosa of a serosa patch may be functionally intact because the presence of nerves suggests that mucosal functions, e.g. resorption and secretion, are under nervous regulation.

Animals↗
PubMed1993

Changes in fluid composition on the serosal surface of jejunum and small colon subjected to venous strangulation obstruction in ponies.

In 6 anesthetized ponies, 3 segments of jejunum and 3 segments of small colon were isolated from the peritoneal cavity in plastic bags filled with Hanks' balanced salt solution. One jejunal and 1 small colon segment were subjected to venous strangulation obstruction for 3 hours (VSO-3), venous strangulation obstruction for 6 hours (VSO-6), or a 6-hour sham procedure to control for changes induced by isolation in a plastic bag. Additional segments of jejunum and colon that were not placed in bags served as controls for histologic examination and collagenase measurements. Samples of fluid surrounding the intestine were obtained for chemical analyses, nucleated cell count, aerobic and anaerobic bacteriologic culture, and measurement of collagenase activity. Full-thickness tissue samples were obtained for histologic examination and measurement of collagenase content. Bacteria did not cross the intestinal wall after 3 and 6 hours of VSO, despite severe mucosal lesions in these segments. At 6 hours, PO2 was significantly less and PCO2 was significantly (P < 0.05) greater in the fluid surrounding the VSO-6 jejunal segments, compared with the sham jejunal segments. The pH was significantly (P < 0.05) less in fluid surrounding VSO-6 small colon segments, compared with the sham colon segments at 6 hours. For jejunum and small colon, phosphate and lactate concentrations were significantly (P < 0.05) greater in VSO-6 fluid than in the corresponding sham fluids at 6 hours. Fibrin formed around all VSO segments, although fibrinogen was not detected in the surrounding fluid, indicating possible rapid conversion of fibrinogen to fibrin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of continuous hyperthermic peritoneal perfusion on prognosis of gastric cancer with serosal invasion.

OBJECTIVE: To evaluate the effects of continuous hyperthermic peritoneal perfusion (CHPP) together with standard chemotherapy on the prognosis of patients with gastric cancer invading the serosa. DESIGN: Retrospective study. SETTING: University hospital, Japan. SUBJECTS: 174 patients who had undergone curative resection for gastric cancer invading the serosa (T3) between 1980 and 1989, 78 of whom had been randomised to be treated with CHPP after operation and 96 who received standard chemotherapy. INTERVENTIONS: CHPP was done immediately after operation; 8-10 l fluid containing 80-100 mg/m2 mitomycin C was perfused at a rate of 100-200 ml/minute, and inflow and out flow temperatures were maintained at 44-45 degrees C and 40-42 degrees C, respectively. This was followed by a standard regimen of mitomycin C and 1-(2-tetrahydrofuryl)-5-fluorouracil/uracil (1:4) (UFT). The control group received the standard regimen only. MAIN OUTCOME MEASURES: Five year survival and patterns of recurrence in three groups: no lymph node metastases, 1-9, and 10 or more. RESULTS: Only in the group with 1-9 lymph node metastases was there an appreciable but not significant difference in 5 year survival: 66% compared with 44% (p = 0.084). The mean disease free survival for patients with peritoneal metastases was 30 months in the CHPP group compared with 23 months among the controls. CONCLUSION: CHPP improved prognosis in patients with T3 gastric cancer who had only 1-9 metastatic lymph nodes.

Aged↗
PubMed2003

Specialized protective role of mucosal glutathione in pigmented rabbit conjunctiva.

PURPOSE: To investigate mechanisms of H(2)O(2)-induced reduction in rates of active ion transport (I(sc)) across the pigmented rabbit conjunctival tissue and the protective role afforded by mucosal glutathione (GSH). METHODS: Changes in I(sc) and specific binding properties of ouabain were evaluated in a modified Ussing chamber setup, using conjunctival tissues freshly excised from pigmented rabbits. Effective concentrations of H(2)O(2) at which 50% of I(sc) was inhibited (IC(50)) were determined for the mucosal and serosal instillation of the agent. The rate of exogenous H(2)O(2) consumption in the mucosal and serosal bathing fluids was estimated. Mucosal 8-Br cAMP at 3 mM, serosal bumetanide at 0.5 mM, and both mucosal and serosal bathing of the conjunctiva with Na(+)-free bicarbonated Ringer's solution (BRS) were used to estimate contributions of conjunctival ion transport mechanisms in I(sc) changes elicited by mucosal H(2)O(2) at IC(50). Specific binding of (3)H-ouabain to the serosal side of the conjunctiva was estimated in the presence of mucosal or serosal H(2)O(2) to assess the role of functional Na(+)/K(+)-ATPase pumps in H(2)O(2) injury. The effect of mucosally instilled GSH and other reductive and nonreductive agents on possible restoration of oxidant-induced decrease in conjunctival I(sc) was also determined. RESULTS: Mucosal and serosal H(2)O(2) decreased conjunctival I(sc) gradually in a dose-dependent manner. The mucosal IC(50) of H(2)O(2)was 1.49 +/- 0.20 mM, whereas the serosal IC(50) was estimated at 10.6 +/- 2.0 micro M. The rate of H(2)O(2) consumption from mucosal fluid was six times faster than that from serosal fluid. Conjunctival tissues pretreated with mucosal H(2)O(2) at IC(50) retained approximately 50% of their maximum 8-Br cAMP-dependent increases in I(sc). Serosal bumetanide did not further reduce the I(sc) beyond the initial 70% decrease caused by mucosal H(2)O(2). When conjunctiva was bathed with Na(+)-free BRS on both the mucosal and serosal sides, before or after addition of mucosal H(2)O(2), the combined effects were additive, decreasing I(sc) by up to 95% to 99%. Mucosal, but not serosal, GSH or reduced L-glutathione mono-ethyl ester (GSH-MEE) superfusion of conjunctival tissues pre-exposed to mucosal H(2)O(2) at IC(50) recovered to 60% to 80% of the initial pre-H(2)O(2) I(sc) after approximately 100 minutes. The specific binding of (3)H-ouabain to the serosal side of the tissue was inhibited by 85% in the presence of mucosal or serosal treatment with H(2)O(2) at their respective IC(50) values. Pretreatment for 60 minutes with either 5 mM GSH, 2 mM GSH-MEE, or 0.1 mM ebselen, when instilled into the mucosal fluid, resulted in 30%, 45%, or 55% reductions, respectively, in ouabain binding after exposure to mucosal H(2)O(2) at IC(50). Furthermore, mucosal posttreatment with 10 mM GSH or 5 mM GSH-MEE of conjunctival tissues pre-exposed to mucosal H(2)O(2) resulted in a 30% recovery of the ouabain-binding level above that observed in tissues exposed to 1.5 mM H(2)O(2) alone on the mucosal side. By contrast, the decrease in conjunctival I(sc) or in the ouabain-binding level elicited by serosal H(2)O(2) at IC(50) was irreversible. CONCLUSIONS: A higher mucosal IC(50) of [H(2)O(2)] on conjunctival I(sc) corresponds to the faster consumption of exogenous H(2)O(2) from mucosal bathing fluid. In addition, actively secreted GSH by conjunctival epithelial cells may help reduce the injury by mucosally applied H(2)O(2). Injury by H(2)O(2) may directly affect vital membrane components (e.g., Na(+),K(+)-ATPase) involved in active ion transport across conjunctiva. Mucosal protection by GSH (or its analogues) of active conjunctival ion transport may be useful in maintaining the physiological functions of conjunctiva under oxidative stress.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

Muscarinic down-regulation of cAMP-stimulated potassium ion secretion by rabbit distal colon.

The sustained effects of the cholinergic agonist carbachol (CCh) on electrolyte transport across the isolated, short-circuited rabbit distal colon were examined in the absence and presence of secretagogue (di-butyryl cyclic-adenosine monophosphate, dB-cAMP). Steady-state, basal absorption of 22Na+, 42K+ (86Rb+), and 36Cl- were not significantly altered by addition of the CCh (10(-4) mmol/l) to the serosal reservoir. Stimulation with dB-cAMP (1.0 mmol/l, serosal) promoted K+ (or Rb+) and Cl- secretion across the colon, without significantly affecting the unidirectional or net fluxes of Na+. Serosal (but not mucosal) addition of CCh to dB-cAMP-stimulated tissues reduced the serosal to mucosal flux of Rb+ (J(Rb)SM) in a concentration-dependent manner with a half-maximum concentration approximately equal 5 micromol/l. Pretreatment with CCh (100 micromol/l, serosal) inhibited dB-cAMP-induced K+ secretion, but had no significant effect on the steady-state unidirectional fluxes of Na+ or Cl-. Serosal histamine (20 micromol/l) also inhibited J(Rb)SM in dB-cAMP-stimulated tissues. Serosal epinephrine (10 micromol/l) promoted a decrease in short-circuit current (Isc) and transepithelial potential (VT) that was mirrored by increases in J(Rb)SM. Both Isc, and VT became more positive and J(Rb)SM was reduced when CCh was added to the epinephrine-stimulated tissues. Serosal muscarine (50 micromol/l) mimicked the CCh-induced inhibition of J(Rb)SM, but serosal nicotine (50 micromol/l) had no effect. In atropine-treated tissues (1 micromol/l, serosal), CCh failed to block dB-cAMP-stimulated increases in J(Rb)SM. The inhibitory action of CCh was observed in tissues that had been pretreated with 50 micromol/l serosal hexamethonium (a ganglionic transmission blocker) or 2 micromol/l serosal tetrodotoxin (a voltage-gated Na+ channel blocker), indicating that the inhibitory action of this cholinergic agonist does not depend on remnant enteric neural pathways. Rubidium ion transport across confluent monolayers of T84 cells was similarly affected by dB-cAMP and CCh, supporting the notion that enteric neural pathways are not required. Serosal charybdotoxin (20 nmol/l) mitigated the inhibitory action of CCh on J(Rb)SM in dB-cAMP-stimulated tissues, suggesting a role for basolateral, Ca2+-dependent K+ channels in the actions of CCh. It is concluded that basolateral muscarinic receptors (and possibly other Ca2+-dependent receptor pathways) of secretory colonocytes mediate the down-regulation of potassium ion secretion by rabbit distal colon, possibly by increasing basolateral membrane K+ conductance.

Animals↗
PubMed1987

Effects of cell volume changes on membrane ionic permeabilities and sodium transport in frog skin (Rana ridibunda).

1. Membrane potential and conductances and short-circuit current were continuously measured with microelectrodes and conventional electrophysiological techniques in a stripped preparation of frog skin epithelium. The effects of the removal of chloride or sodium ions and the concentration or dilution of the serosal (inner) bathing solution were studied. 2. Chloride- or sodium-free solutions produced a cell depolarization of about 30 mV in parallel with a fall in the short-circuit current. Mucosal and serosal membrane conductances both decreased and the sodium permeability of the mucosal barrier was calculated to fall to about one-half its value in standard Ringer solution. The observed decrease in the short-circuit current is probably related to the combined effect of the decrease in sodium permeability and the decrease in the driving force across the mucosal membrane. 3. The removal of chloride or sodium ions reduced the depolarization caused by serosal perfusion with high-potassium solutions (50 mM-KCl). The ratio of the change in cell membrane potential under short-circuit conditions to the change in the potassium equilibrium potential (delta Ec(s.c.)/delta EK), was 0.59 in standard Ringer solution and 0.26 and 0.24 after the removal of chloride or sodium respectively. The depolarizing effect of barium-containing solutions (2 mM-BaCl2) was also markedly reduced in chloride- or sodium-free solutions, suggesting a decrease of the potassium selectivity of the serosal membrane in these conditions. 4. Increasing the osmolality of the serosal bathing solution produced similar effects, i.e. cell depolarization, fall in the short-circuit current and membrane conductances and reduction of the depolarizing effect of high-potassium and barium solutions. On the contrary, dilution of the serosal bath produced the opposite effects, consistent with an increase in the serosal permeability to potassium. 5. The effects of chloride- or sodium-free solutions were reversed by the dilution of the serosal bath. Cells repolarized when exposed to low-osmolality solutions after being in the absence of serosal chloride or sodium. The repolarization ran in parallel with the restoration of the short-circuit current and the potassium selectivity of the serosal membrane. 6. The results show that the effects produced by the removal of sodium or chloride ions from the serosal bathing solution are most probably mediated by a reduction in cell volume. Cell volume changes would lead to changes in the serosal membrane selectivity to potassium and thus to changes in cell membrane potential and sodium transport.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1984

Effects of histamine and histamine receptor antagonists on ion transport in rabbit descending colon.

The effects of histamine on colonic ion transport were examined in in vitro preparations of rabbit descending colon. Serosal addition of histamine (10(-5) M) produced a transient increase in short-circuit current (Isc) and transepithelial conductance. The Isc response to histamine could be blocked by removing Cl from both bathing solutions, adding furosemide (10(-3) M) to the serosal bathing solution, adding indomethacin to the serosal and mucosal bathing solutions (10(-5) M), or removing Ca from the serosal bathing solution. In addition, the histamine-induced increase in Isc was inhibited in a dose-dependent manner by the H1-receptor antagonist diphenhydramine, with a maximal inhibition at 10(-4) M and a half-maximal inhibition at 3 X 10(-7) M. The H2-receptor antagonist cimetidine (10(-3) M) was without effect on the histamine response. Measurement of unidirectional Na, K, and Cl fluxes revealed that serosal addition of diphenhydramine (10(-3) M) reduced basal Isc due to a decrease in mucosal-to-serosal Na flux. Serosal addition of diphenhydramine (10(-3) M) also inhibited the increase in Isc produced by serosal addition of prostaglandin E1, 8-bromo-cAMP, cholera toxin, or the ionophore A23187. Measurement of unidirectional K and Cl fluxes revealed that prostaglandin E1 alone increased serosal-to-mucosal K and Cl fluxes and reduced the mucosal-to-serosal K flux, thereby increasing net K and Cl secretion. Serosal diphenhydramine (10(-3) M) abolished the changes in Cl fluxes produced by prostaglandin E1 and reduced the magnitude of the changes in K fluxes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Concentration-dependent effects of disulfonic stilbenes on colonic chloride transport.

Stripped rabbit colonic mucosa was studied in vitro in Ussing chambers to determine effects of the disulfonic stilbenes 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS) and 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) and the diuretic furosemide on unidirectional and net Cl fluxes. Results from these studies reveal that SITS (1 mM) added to either the serosal or mucosal bathing solution reduced both unidirectional Cl fluxes with no significant change in net Cl flux. The effects of SITS do not appear to be mediated by an effect on the shunt permeability since SITS (1 mM) did not alter either the intercept or slope of the Na concentration dependence of the serosal-to-mucosal Na flux. Furosemide (1 mM) decreased the serosal-to-mucosal Cl flux without altering short-circuit current (Isc) when added to the luminal bathing solution and reduced both unidirectional fluxes and increased Isc when added to the serosal bathing solution. DIDS (0.5 mM) added to the luminal bathing solution did not alter unidirectional Cl fluxes or Isc. However, serosal addition of DIDS produced dose-dependent changes in Cl transport. At 5 microM DIDS reduced the mucosal-to-serosal Cl flux without altering the serosal-to-mucosal flux or Isc. At 50 microM DIDS reduced the mucosal-to-serosal Cl flux and increased Isc, and at 0.5 mM DIDS increased the serosal-to-mucosal Cl flux, reduced the mucosal-to-serosal Cl flux, and increased Isc and transepithelial conductance. The effect of 0.5 mM DIDS on Isc was reduced by Ca removal from the serosal bathing solution and by the loop diuretics furosemide and bumetanide.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1980

Effects of cyclic AMP, ouabain and furosemide on ion transport in isolated canine gastric mucosa.

1. Cyclic AMP (10 mM), present in the serosal solution of isolated dog gastric mucosa, increased potential difference (p.d.), short-circuit current (ISC), net flux of Na+ from the mucosal to serosal side, and the unidirectional flux of K+ from the mucosal to serosal side. Cyclic AMP did not stimulate H+ or Cl- secretion. 2. Dibutyryl cyclic AMP (DBcAMP, 1 mM) or theophylline (2 mM), present in the serosal solution, stimulated H+ and Cl- secretion, decreased p.d., ISC and electrical resistance. These compounds had no effect on Na+ transport. The stimulatory effect of DBcAMP on H+ secretion was still present after pretreatment with cimetidine or atropine. 3. Ouabain abolished both the p.d. and ISC of the histamine-stimulated gastric mucosa. The mucosal to serosal flux of Na+ and the serosal to mucosal flux of Cl- were significantly decreased in the presence of ouabain. Ouabain caused an increase in the serosal to mucosal flux of K+ and high concentrations caused a significant reduction in H+ secretion. 4. Furosemide (10(-4) M) decreased p.d., ISC and net flux of Na+. Higher concentrations inhibited the net flux of Cl- from the serosal to mucosal side. 5. These results suggest that in isolated dog gastric mucosa, (1) both DBcAMP and theophylline may increase intracellular cyclic AMP to stimulate H+ and Cl- secretion, (2) cyclic AMP, outside the serosal membrane, stimulates active transport of Na+; in contrast, ouabain inhibits this active process predominantly, (3) the selective action of furosemide on Na+ transport indicates that Na+ and Cl- move via separate transport pathways across the serosal border.

Animals↗
PubMed1988

The transport and metabolism of naturally occurring pyrimidine nucleosides by isolated rat jejunum.

1. Uridine perfused through the lumen of isolated loops of rat jejunum over a concentration range of 0.1-1.0 mM gave rise to higher serosal concentrations of uracil than the equivalent luminal concentration of uracil (P less than 0.001). No serosal uridine could be detected. 2. Luminal thymidine over a concentration range of 0.1-0.5 mM gave rise to the same serosal concentration of thymine as the equivalent luminal concentration of thymine (P greater than 0.1). Low concentrations of serosal thymidine were detected. Both luminal thymidine and thymine gave rise to elevated levels of serosal uracil. 3. Luminal cytidine at concentrations of 0.1-0.5 mM was poorly transported and yielded low serosal concentrations of cytidine. No serosal cytosine was detected, although elevated levels of uracil were found in the serosal secretions. 4. Cytosine over a luminal concentration range of 0.1-0.5 mM gave rise to low concentrations of cytosine in the serosal secretions. These results were consistent with a passive diffusion model for cytosine transport. No increase in serosal uracil was detected. 5. The cleavage of uridine and thymidine to their respective pyrimidine bases occurred via a cytoplasmic nucleoside phosphorylase, which had a similar Michaelis constant (Km), (61.0 +/- 4.4 and 97.1 +/- 5.7 microM for uridine and thymidine, respectively) but a maximal velocity (Vmax) for uridine cleavage (320 +/- 32 nmol min-1 (mg protein)-1) 13 times that for thymidine cleavage (24.7 +/- 1.4 nmol min-1 (mg protein)-1). 6. The differences between the three pyrimidine nucleosides are discussed with reference to the interactions between their epithelial transport and metabolism.

Animals↗
PubMed1985

Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

The present studies probe the role of Ca2+ and Na+ in the stimulation-permeability coupling sequences by which antidiuretic hormone (ADH) induces a cyclic AMP (cAMP)-mediated increase in urea permeability in toad urinary bladder. The following results were obtained: (a) Removal of mucosal Na+ or Ca2+ or deletion of serosal Ca2+ did not modify ADH action. (b) Reduction of the serosal Na+ concentration to less than 50 mM inhibited the effects of both ADH and cAMP. The minimal concentration of serosal Na+ needed for the hormone to elicit its maximal effect was reduced to approximately 10 mM if serosal Ca2+ was concomitantly deleted. (c) The Na+ ionophore monensin produced an inhibition of ADH and cAMP actions that was dependent on the presence of Na+ and Ca2+ in the serosa. (d) The Ca2+ ionophore A23187 produced a serosal Ca2+-dependent inhibition of ADH effect and did not modify cAMP action. (e) Carbachol, which increases Ca2+ uptake to the same extent that A23187 does, had no effect on ADH action. (f) Quinidine, which releases Ca2+ from intracellular stores, produced a large inhibition of the action of ADH but not that of cAMP; the inhibition was greatly reduced if serosal Ca2+ was deleted. (g) Dinitrophenol and iodoacetate, which also release Ca2+ from intracellular pools, had no effect on ADH action. (h) The Ca2+ channel blocker diltiazem had no effect on ADH action and did not modify the inhibitions produced by deletion of serosal Na+ or monensin. (i) The cyclooxygenase inhibitor indomethacin partially removed the inhibition produced by deletion of serosal Na+ and almost completely impeded the inhibitions produced by either monensin or A23187. It is concluded: (a) Extracellular Ca2+, Na+ transport rates, and serosal Na+, in concentrations between 10 and 110 mM, have no participation in modulating the increase in urea permeability produced by ADH. (b) Increases in cytosolic Ca2+ activity, which are capable of inhibiting the effect of ADH on urea permeability at pre- and/or post-cAMP steps, seem to be highly compartmentalized. (c) Endogenous prostaglandins might play a role in the inhibitions produced by absence of serosal Na+, monensin, or A23187.

Animals↗
PubMed2000

Elevated serum CA-125 levels in hemodialysis patients with peritoneal, pleural, or pericardial fluids.

OBJECTIVE: Serum CA-125, an ovarian tumor marker, is used especially in the follow-up of ovarian cancer for monitoring the efficacy of therapy and for early detection of recurrence. A number of benign gynecologic as well as benign and malignant nongynecologic conditions are associated with elevated serum CA-125 levels. Malignant and nonmalignant serosal fluids were also found to be associated with high serum levels of CA-125, suggesting that the presence of fluid in the serosal cavities may stimulate its release. METHODS: We performed a clinical study in 39 patients (21 females, 18 males) on chronic hemodialysis who were divided into two groups based on the presence of fluid in the serosal cavities (peritoneum, pleura, or pericardium) without clinical and radiologic evidence of neoplasia. There were 26 patients (16 females, 10 males) aged 50.11 +/- 13.86 years (range, 20-76 years) in the serosal fluid-negative group (group 1) and 13 patients (8 females, 5 males) aged 45.30 +/- 18.84 years (range, 17-73 years) in the serosal fluid-positive group (group 2). The control group consisted of 52 healthy volunteers (30 females, 22 males) aged 44.19 +/- 12.59 years (range, 19-68 years). RESULTS: Significantly elevated serum CA-125 levels were found in hemodialysis patients with serosal fluid (P < 0.05) when compared with both the hemodialysis patients without serosal fluid and the control group. There was no statistically significant difference between the control group and the patients without serosal fluids (P > 0.05). CONCLUSION: Although CA-125 can be considered a reliable tumor marker in patients undergoing hemodialysis, it should be interpreted with caution in patients with serosal fluids.

Adult↗
PubMed1982

Steady states and the effects of ouabain in the Necturus gallbladder epithelium: a model analysis.

A simple numerical model for the Necturus gallbladder epithelium is presented. K+, Na+ and Cl- cross the mucosal and serosal membranes as well as the junctions by means of electrodiffusion; furthermore the mucosal membrane contains a neutral entry mechanism for NaCl and the serosal membrane contains an active pump for K+ and Na+. The values which have been used for the model are taken from the literature. The model can only attain steady states if the resistance of the serosal membrane is lower than 1000 omega cm2. Values reported in the literature for the resistance of this membrane vary from about 3000 to about 100 omega cm2. We shall argue, however, that the higher estimates are in error because they are derived from a model of the tissue in which each membrane and the junction are modeled by a resistor; this procedure is invalid because the resistance of the lateral intercellular space relative to the resistance of the tight junctions is neglected and consequently the resistance of the serosal membrane is overestimated by a factor of about four. Apart from predicting a realistic steady state at normal external concentrations the model can predict quantitatively several experimental results obtained from the living epithelium. We have focused on the experiments which test the permeabilities of the serosal membrane and the properties of the pump: i) Replacement of serosal Cl- by an impermeant ion. ii) Replacement of serosal K+ by Na+. iii) Inhibiting the (Na+, K+)-pump. The best correspondence between model and experiments is obtained when the pump is assumed to be electrogenic (or rheogenic) with a ratio of coupling between Na+ and K+ of 3:2. In this case both model and direct experiments (also presented in this paper) show an initial abrupt depolarization of 6 to 7 mV. The model also shows that it cannot be concluded from i and ii that the Cl- permeability of the serosal membrane is low. The model explains, even with high passive Cl- permeabilities, why the intracellular Cl- concentration is relatively unaffected by paracellular currents, a fact which in other epithelia has been taken as an implication of a low Cl- permeability of the serosal membranes.

Animals↗
PubMed1993

Rabbit esophageal cells possess K+ channels: effect of hyposmotic stress on channel activity.

BACKGROUND: In many cell types, basolateral K+ channels are important in maintaining transepithelial Na+ absorption and regulatory volume decrease (RVD) after hyposmolar stress. However, in the esophagus the effect of K+ transport in maintaining baseline short-circuit current (SCC) (Na+ absorption) and RVD is unknown. METHODS: Ussing chambers were used to evaluate changes in SCC of rabbit esophageal mucosa in response to serosal Ba2+ (4 mmol/L), quinine (1 mmol/L), and increasing serosal [K+]. To determine whether K+ channel(s) are activated in RVD, changes in SCC in response to serosal hyposmolarity (156 mOsm) were assessed in the presence or absence of serosal quinine. RESULTS: Serosal Ba2+, quinine, or increased serosal [K+] caused a decline in baseline SCC. Serosal hyposmolarity caused an increase in SCC that was not blocked by mucosal application of amiloride (10(-4) mmol/L). In contrast, serosal quinine completely blocked the hyposmolar-induced increase in SCC. CONCLUSIONS: These studies suggest that rabbit esophageal cells possess Ba(2+)- and quinine-sensitive basolateral K+ channel(s) that are active under baseline conditions. Potassium conductance(s) also appear to be activated by external serosal hyposmolarity and may be involved in the process of RVD.

Amiloride↗
PubMed1996

Ammonia transport by the urinary bladder of Bufo marinus.

All experiments were performed in vitro on toad bladders. Bladder sacs from acidotic toads produced a concentration gradient across the bladder with both [NH3] and [NH4] higher in the mucosal media. By varying the pH of the serosal media, paired sacs from normal toads were incubated with similar [NH3] in the serosal media but a 75 fold difference in [NH4] of the serosal media of the pairs. The hemibladders with the higher [NH4] had a 2.4 fold greater excretory flux than the paired sac. Both serosal to mucosal and mucosal to serosal fluxes were determined in normal bladders between chambers at various ammonium concentration gradients. The plot of mucosal to serosal flux against concentration produced a curve compatible with both carrier mediated and diffusion transport; the plot of serosal to mucosal flux produced a straight line with flux increasing when the ammonium concentration was increased. The serosal to mucosal transepithelial flux was augmented by making the serosal side of the bladder 50 mV positive. Although NH3 diffusion may occur, it cannot be the primary method of ammonia transport in the toad bladder.

Ammonia↗
PubMed1994

Osmotic water flow pathways across Necturus gallbladder: role of the tight junction.

To explore the quantitative significance of passive water flow through tight junctions of leaky epithelia, transepithelial water flow rates were measured in Necturus gallbladder mounted in chambers. Osmotic flows generated by raffinose gradients were asymmetrical with the greater flow in the mucosal-to-serosal direction. In tissue fixed in situ, intercellular spaces were dilated during mucosal-to-serosal flow and closed during serosal-to-mucosal flow. Tight junctions were focally separated (blistered), which correlated with the magnitude of mucosal-to-serosal flow. Blisters were not observed during serosal-to-mucosal flow or in nontransporting gallbladders. In freeze-fracture replicas, blisters appeared as pockets between intramembranous strands. Protamine, which decreases electrical conductance and increases depth and complexity of the tight junction, reduced osmotic water flow by approximately 30% in the mucosal-to-serosal direction (100 mosmol/kg gradient) without altering serosal-to-mucosal flow. We suggest that in the steady state, at least 30% of osmotically driven water passes transjunctionally in the mucosal-to-serosal direction, but flow is transcellular in the serosal-to-mucosal direction. Directionally divergent pathways may account for flow asymmetry.

Animals↗