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PubMed1990

The effect of calcium on gallbladder absorption.

The absorption of water and electrolytes is an important physiologic function of the gallbladder which is altered during gallstone formation. Extracellular calcium and calcium channel antagonists are known to affect intestinal absorption, yet their effect on gallbladder absorption is less well defined. We, therefore, tested the hypothesis that changes in extracellular calcium or in calcium channels would alter gallbladder absorption. New Zealand white rabbit gallbladders were removed, filled with a modified Krebs buffer (Ca2+ = 0.7 mM), and suspended in an oxygenated bath of the same buffer. Water absorption was determined gravimetrically by obtaining serial gallbladder weights at 10-min intervals. After a 40-min control period, the serosal bathing solution was changed to one of four experimental solutions (n = 6 for each group): Ca2+ = 0.25, 0.7, or 1.2 mM or Ca2+ = 0.7 mM plus 0.1 mM verapamil. Absorption was determined during an 80-min experimental period with results expressed as the percentage change in gallbladder absorption compared to that of the control period. The 0.25, 0.7, and 1.2 mM Ca2+ groups did not show a significant change in absorption rate from their respective control rates. However, the verapamil group did demonstrate a significant (P less than 0.05) decrease in absorption rate of -69 +/- 8% by the end of the experimental period. These data demonstrate that verapamil inhibits gallbladder absorption while changes in serosal calcium concentration have no effect. We conclude that calcium channels and intracellular calcium may play an important role in modulating gallbladder absorption.

Absorption↗
PubMed1987

Exogenous ATP-stimulated calcium uptake in isolated rat intestinal epithelial cells.

ATP in the extracellular medium is known to stimulate Ca uptake into avian intestinal epithelial cells. We have now demonstrated a similar effect of ATP in mammalian intestinal epithelial cells and have further characterized this effect. Exogenous ATP increased 45Ca uptake 2-6 fold in isolated rat small intestinal epithelial cells, with a maximal effect at 1 mM and an ED50 of 290 microM. A strict structural requirement for nucleotide-stimulated 45Ca uptake was observed. ADP was much less effective than ATP and gamma-thio-ATP, and 5'-AMP, cyclic AMP, adenosine, non-adenine nucleotides, non-hydrolyzable ATP analogs and ATP analogs with ring substitutions at the 8 position were inactive. Prenylamine (100 microM) completely inhibited ATP-stimulated 45Ca uptake, while verapamil (100 microM) had only a small effect. In the intact intestine, ATP increased short-circuit current (Isc) when added to the mucosal side of the tissue. This effect was reduced by 10 microM and abolished by 100 microM prenylamine. The effect of ATP on Isc was markedly reduced in Cl-free solutions and in reduced-Ca solutions. Serosal and mucosal addition of the nonhydrolyzable ATP analog, beta, gamma-methylene-ATP, and serosal addition of ATP had little or no effect on Isc. The similarities between the effects of ATP in isolated cells and in the intact intestine suggest that the effect of ATP on Isc may be at least partially mediated through stimulation of Ca uptake into the epithelial cells.

Adenosine Triphosphate↗
PubMed1988

The neurosecretory effect of ouabain on isolated rabbit ileal mucosa.

Ouabain, when added to fluid bathing rabbit ileal mucosa mounted in a flux chamber, transiently increases short circuit current, implying a paradoxical secretory response. To determine the cause of this change, we studied unidirectional fluxes of 36Cl and 23Na and the effects of ion substitution, of reduced Ca concentration, verapamil, tetrodotoxin and atropine. Ouabain 0.1 mM, transiently increased the serosal to mucosal flux of Cl and Na, increased Isc and PD and reduced ion conductance. The Isc response to ouabain was diminished by reducing the bath fluid concentration of Cl, of Ca, and by adding verapamil. Tetrodotoxin both delayed and reduced the maximal Isc response; atropine had no effect. We conclude that ouabain acts by releasing a neurotransmitter of unknown identity and by increasing the serosal to mucosal flux of Cl.

Animals↗
PubMed1992

Association of radiolabeled urogastrone binding with regenerating intestinal mucosa and epidermal growth factor/urogastrone producing organs in rat.

In the present study, we have tested the hypothesis that the regeneration of intestinal epithelium is regulated by changes in the uptake of radiolabeled recombinant human urogastrone (125I rhUG) in the regenerating mucosa and epidermal growth factor/urogastrone (EGF/URO) producing organs in the rats. Operations were performed on rats to approximate the ileal mucosa to the serosal surface of the cecum. This procedure allows the regeneration of ileal mucosa onto the serosal surface of the cecum. Groups of 5 rats were killed on the 2nd, 4th, 8th and 12th post-operative days. Two hours before autopsy, rats were given 0.5 ml (50 microCi with 30 micrograms protein) of 125I rhUG intravenously and the following tissues were removed: regenerating mucosa, salivary gland, duodenum, liver and kidney. Results indicated that the uptake of 125I rhUG was significantly greater in the salivary gland and duodenum on the 2nd post-operative day which gradually tapered with increasing time after surgery. A similar pattern in the uptake of 125I rhUG was also evident in the regenerating mucosa. Further analysis revealed a significant correlation between the uptake of 125I rhUG in the salivary gland and duodenum vs rate of epithelialization and uptake of 125I rhUG in the regenerative mucosa. These results suggested that the endogenous EGF/URO produced in the salivary gland and duodenum may be a factor in the regulation of intestinal regeneration; however, the mechanism responsible for reflex stimulation of EGF/URO production in these organs is not known.

Animals↗
PubMed1993

Postoperative adhesion after uterine horn surgery in the rat, with the use of TC7.

The influence of TC7 in adhesion prevention was tested on 24, 2.5-month-old Wistar rats. Their right and left uterine horns were homogeneously allotted into four experimental groups, each of 12 horns. The groups were as follows: Group C (n = 12), that underwent cuts along 1 cm in the serosal layer; Group TC (n = 12), where the uterine horn was only surrounded with 3 layers of TC7, 1 x 1 cm in size; Group C+TC (n = 12) in which the serosal cuts were covered with TC7, as in group TC and an untouched control group (n = 12). All uterine horns were kept in uniform contact with the intestinal serosa layer by means of two 8/0 nylon stitches spaced 2 cm apart, so that the adhesion surfaces were the same in all groups. Lengths in mm and severity adhesions (0 = no adhesion to 3 = severe adhesion) were recorded. The injury in group C caused extensive (8.83 +/- 4.77 mm) and dense adhesions (score 2.42 +/- 1.11) in 83.33% of the cases. No significant differences were observed compared with the C+TC group (8.08 +/- 5.45 mm, score 2.25 +/- 1.30; P > 0.05, ANOVA). Significantly, more adhesions were observed on the C and C+TC Groups than in the control (1.00 +/- 2.27 mm, score 0.16 +/- 0.37) and TC (3.08 +/- 3.38 mm, score 1.00 +/- 1.15) groups (P < 0.05, ANOVA). TC7 does not appear to be an effective agent for preventing postoperative adhesions in this animal model.

Analysis of Variance↗
PubMed1986

Calcium-modulated desmosome formation and sodium-regulated keratinization in frog skin cultures.

The processes of desmosome formation and keratinization were studied in isolated frog skins cultured in a two-compartment (mucosal and serosal) chamber. Before culture, the skin fragments were trypsinized (stratum corneum together with some parts of stratum granulosum and spinosum were scraped off with forceps) allowing the stratum germinativum to remain on the dermis. When both the mucosal and the serosal culture media contained 1.5 mM calcium and 86 mM sodium concentrations, fully developed desmosomes were differentiated and no keratinization occurred. When the mucosal medium was lowered in two steps to a final calcium concentration of 0.5 mM by dilution with tridistilled sterile water, poorly developed desmosomes were formed, keratinocytes interdigitated and the keratinization was strongly enhanced. The calcium-dependent desmosome formation was affected by the salt gradient established across the skin. These two effects, modulated desmosome formation (calcium) and increased keratinization (sodium), were concomitant with but did not complement one another.

Animals↗
PubMed1986

Antidiuretic hormone response in the amphibian urinary bladder: time course of cytochalasin-induced vacuole formation, an ultrastructural study employing ruthenium red.

Cytochalasin is known to inhibit the antidiuretic hormone-induced hydro-osmotic response (bulk water flow) in the amphibian urinary bladder without altering hormone-stimulated diffusional water permeability or short-circuit current. In addition, histological studies have shown that the mold metabolite induces the formation of large intracellular vacuoles or lakes in the epithelial cells. We report here a transmission electron microscopic time-course study which indicates that during the early phases of the ADH response cytochalasin causes the formation of numerous multivesicular bodies or aggregates derived from individual basolateral pinocytotic vesicles. Because of their apparent hypertonic nature, the vesicles, as well as the vesicular aggregates, accumulate water during hormone-stimulated hydro-osmotic flow. As a result, the multivesicular bodies dilate and fuse to form the large intracellular lakes characteristic of cytochalasin treatment in the presence of both an applied osmotic gradient and vasopressin. In the presence of mucosal ruthenium red, the luminal glycocalyx was heavily stained with this tracer. At no time, however, even in the presence of hormone, was there any evidence for the uptake of this dye at the apical epithelial border. In the presence of serosal ruthenium red, the lateral intercellular spaces, basolateral pinocytotic vesicles, basal lamina, and collagen, as well as other subepithelial structures, were ruthenium positive. With cytochalasin D, vasopressin, and serosal ruthenium red, both the pinocytotic vesicles and the multivesicular bodies demonstrated an apparent membrane associated ruthenium positive coat. The tracer data indicates that the basolateral pinocytotic vesicles, increased by the presence of hormone, are indeed endocytotic in nature. The mucopolysaccharide coat associated with these structures may be involved in ionic and/or fluid transport.

Animals↗
PubMed1989

Characterization of mitomycin C-induced gastrointestinal damage. II. In vitro everted sac experiment.

The everted gut sac technique was employed to clarify the effects of preadministration of mitomycin C (MMC) on intestinal transport of various drugs. Loss of intestinal tissue weight and increase in mucosal-to-serosal fluxes of passively absorbed drugs were noted in the case of MMC pretreatment, although the extent of the latter effect varied according to the inherent absorbability of each drug. The maximal effect of MMC on intestinal tissue weight and transport of sulfanilamide, a model of a passively absorbed drug, was observed 48 hr after pretreatment. The increase in the transfer of sulfanilamide correlated well with the MMC-induced decrease in intestinal tissue weight. These phenomena may result from the shortened transfer distance from mucosal to serosal fluid and impaired barrier function of the intestinal mucosa. On the other hand, transport of actively absorbed 3-O-methyl-D-glucose was not influenced by MMC pretreatment, which could be explained by an increment in the passive permeation counterbalancing the decrement in the active permeation. The present study also suggested that the measurement of transport of drugs through everted gut sacs might be useful as a simple and qualitative index of gastrointestinal mucosal damage.

3-O-Methylglucose↗
PubMed1991

Selected human immunodeficiency virus replicates preferentially through the basolateral surface of differentiated human colon epithelial cells.

We have used HIV1-NDK-infected HT29 cells grown on permeable substratum to study the polarity of virus maturation in human intestinal cells. When cultured in glucose-containing medium, these cells are mostly undifferentiated. The removal of glucose from the medium allowed the emergence of a selected differentiated subpopulation which continued to produce viral particles in the culture supernatant. The polarity of viral production was evaluated by harvesting virus from the two sides of the monolayer. Seventy-five percent of released HIV was found on the basolateral side of the monolayer. Mature viral particles were observed by electron microscopy near the apical (luminal) and the basolateral (serosal) membrane. These data suggest that epithelial cells of the colon productively infected by a selected strain of HIV are able to produce the virus through both sides of the epithelium but mainly through the serosal side.

Cell Differentiation↗
PubMed1980

Inhibition of ADH-enhanced transepithelial urea and water movement by prostaglandins.

The effects of PGF2 alpha and PGE2 on transepithelial urea flux and osmotic water flow were evaluated in total bladders. Mucosal to serosal urea flux and osmotic water flow were not changed from basal values by the addition of either prostaglandin to the serosal bath. However, treatment with either PGF2 inhibited both urea flux and osmotic water flow in response to ADH stimulation in a concentration-dependent manner. The hydrosmotic response to ADH was more sensitive to prostaglandin inhibition than was urea flux. The inhibitory effect of the prostaglandins on ADH-enhanced urea flux was not dependent upon inhibition of the hydrosmotic response, since both PGF2 alpha and PGE2 decreased urea flux in the absence of a transepithelial osmotic gradient. Prostaglandin E2 was a more potent inhibitor than PGF2 alpha of both ADH-enhanced urea flux and osmotic water flow. The PGF2 alpha antagonism of osmotic water flow was apparently competitive, while antagonism of urea flux was apparently noncompetitive. The results are consistent with the hypothesis of the existence of a "spare" population of prostaglandin receptors that modulate water flow, but the absence of a "spare" prostaglandin receptor population with respect to the modulation of urea flux.

Animals↗
PubMed1989

Effect of fish-fat or beef-fat supplemented diet on immune complex-induced enteropathy in the rat.

In contrast to animals on a beef fat-supplemented diet (BFD), animals maintained on a fish fat-supplemented diet (FFD) incorporate increased amounts of eicosapentaenoic acid (EPA) into membrane phospholipids. Generation of lipid mediators from such tissues favors the formation of compounds with less pro-inflammatory activity than are derived from tissues poor in EPA. Nevertheless, the FFD has not had a uniformly beneficial effect on animal models of inflammatory diseases. We previously showed that intravenous injection of rat anti-BSA-BSA complexes (IC) prepared in 5x antigen excess rapidly induced a striate pattern of serosal (to mucosal) hemorrhage and vascular congestion throughout the small intestine. In this study, we tested the effect of a BFD and FFD on immune complex-induced enteropathy. After six (Expt. 1) or eight weeks (Expt. 2) on the diet, rats were injected with IC and the severity of serosal hyperemia in the small intestine was scored. In some FFD, no lesions were seen under conditions which elicited moderate to severe lesions in BFD rats. In Expt. 1 involving 22 rats and in Expt. 2 involving 28 rats, those on the FFD had a significantly lower composite lesional score compared to those on the BFD, p less than 0.005 and p less than 0.005, respectively. These results indicate that the FFD had a beneficial effect on IC-induced enteropathy. It is suggested that this effect of the FFD may be mediated primarily by a reduction in availability of platelet-activating factor.

Animals↗
PubMed1988

Transport pathways in rat lingual epithelium.

Measurements of ion transport across isolated lingual epithelium of rat were correlated with electrophysiological recordings from taste nerves. At hyperosmotic concentrations of NaCl, sodium ions enter the mucosal membrane of the isolated epithelium partially through an amiloride-inhibitable pathway and exit the serosal membrane through a Na+-K+-ATPase. At hyposmotic concentrations of KCl, potassium ions enter the mucosal membrane through a K+ pathway that is inhibited by 4-aminopyridine and exit at the serosal membrane through a K+ pathway that is inhibited by BaCl2. The inhibition of sodium transport by amiloride and potassium transport by 4-aminopyridine is consistent with previously published electrophysiological recordings from the chorda tympani nerve bundle (CT) and recordings from nucleus of the solitary tract (NST) obtained here. The responses to NaCl are greater than the responses to KCl at equimolar concentrations over the entire concentration range both in epithelial and neural measurements. At hyposmotic concentrations of NaCl the epithelial responses include inward sodium and outward chloride components. Isolated rat tongue is only slightly stimulated by D-glucose or sucrose as are the CT and NTS responses. These data suggest that events in taste transduction can be understood, in part, by measuring the epithelial responses of isolated rat tongue.

4-Aminopyridine↗
PubMed1990

The myenteric plexus regulates cell growth in rat jejunum.

The roles of the myenteric and extrinsic nerves in the control of proliferation and cell growth in the rat jejunum were studied. The myenteric plexus and/or the extrinsic nerves in a segment of rat jejunum were ablated by serosal application of the surfactant benzyldimethyltetradecylammonium chloride or by crushing the nerves passing through the mesentery, respectively. Ablation of both myenteric and extrinsic nerves, but not the extrinsic nerves alone, resulted in a significant increase in the mitotic rate of the crypt-epithelial cells and in the size of VIP-immunoreactive neurons in the submucosal plexus. The increased mitotic rate was correlated with an increase in the weight of the mucosa per unit length of gut and in the villus length and crypt depth. Neither extrinsic denervation alone nor serosal application of saline had any effect on these parameters. Our results suggest that the myenteric plexus is able to influence the rate of cell proliferation and cell growth in the rat jejunum.

Animals↗
PubMed1991

Mucosal distortion by compression elicits polarized reflexes and enhances responses of the circular muscle to distension in the small intestine.

The possibility that distortion of the mucosa by compression might be a sufficient stimulus to evoke reflex responses in intestinal muscle, and that such reflexes might summate with distension-evoked (stretch) reflexes, was tested in isolated segments of guinea pig small intestine. Opened segments of intestine were pinned flat in an organ bath with, or without, distending balloons embedded in its base. Intracellular microelectrode recordings were taken from the circular muscle oral and anal to sites of application of sensory stimuli. Pressure against the mucosa, which distorts the villi without the wall being stretched, evoked polarized reflex responses in the circular muscle, consisting of excitatory junction potentials oral and inhibitory junction potentials anal to the stimulus. Distension stimuli applied by 6-mm diameter balloons that pushed against either the serosal or the mucosal surface also evoked excitatory junction potentials in the muscle oral to the stimulus and inhibitory junction potentials at anal sites. Response amplitudes were 20% greater when the distending balloon pushed against the mucosal surface. Responses to distension from the serosal side were of 20% greater amplitude when combined with mucosal distortion by compression than without such compression. It is concluded that peristaltic movements that are commonly studied in the small intestine can be consequences of reflexes elicited at the same time from mucosal distortion receptors and from stretch receptors.

Animals↗
PubMed1981

Release of vasoactive intestinal polypeptide by electrical field stimulation of rabbit ileum.

The release of vasoactive intestinal polypeptide (VIP) induced by electrical field stimulation (EFS) of rabbit ileum was studied in vitro. EFS parallel to the muscularis propria caused a significant increase in VIP concentration in the buffer bathing the serosal surface of full-thickness ileum. This effect was blocked by 10(-7) M tetrodotoxin. When circular and longitudinal muscle was removed, the amount of measurable VIP in the tissue decreased to about one-half that of full-thickness ileum, and EFS no longer caused release of VIP into the serosal or mucosal buffers. Our data indicate that EFS of rabbit ileum causes release of VIP, presumably form VIP-containing nerves present in the tissue. These results support the idea that VIP may be a physiological neuroregulator of intestinal function.

Animals↗
PubMed1987

Neuropeptide modification of chloride secretion in guinea pig distal colon.

This study examined the effects of electrically stimulating submucosal neurons in the guinea pig isolated distal colonic mucosa and determined the effects of several peptides that are present in these neurons. Electrical field stimulation of muscle-stripped segments of guinea pig distal colonic mucosa, set up in Ussing flux chambers, evoked an increase in short-circuit current (Isc), of 371 +/- 31 MicroA.cm-2. The response to electrical stimulation was abolished by tetrodotoxin and significantly reduced by serosal furosemide. Atropine reduced, but did not abolish, the neurally evoked response. Addition of neuropeptide Y and galanin to the serosal bath had no effect on baseline Isc, but both evoked a concentration-dependent decrease in the neurally evoked secretory response. Vasoactive intestinal polypeptide evoked a concentration-dependent increase in basal (unstimulated) Isc that was reduced by furosemide and unaltered by tetrodotoxin. Neuropeptide Y, but not galanin, significantly reduced the secretory responses to vasoactive intestinal polypeptide and bethanechol. Somatostatin 201-995 and human calcitonin gene-related peptide had no effect on basal Isc nor did either alter the neurally evoked response. These results suggest that acetylcholine and non-cholinergic neurotransmitter(s) stimulate chloride secretion in the guinea pig distal colonic mucosa. This neurosecretory response may be modulated by neuropeptide Y and galanin that are found within submucosal neurons.

Animals↗
PubMed1988

Actions of gastrin-releasing peptide and related mammalian and amphibian peptides on ion transport in the porcine proximal jejunum.

The 27-amino acid peptide gastrin-releasing peptide (GRP) and the decapeptide neuromedin B (NMB) are structurally related to bombesin (BB) and exist within the mammalian small intestine. We examined the actions of porcine GRP and NMB on ion transport in the porcine proximal jejunum in vitro and compared their activities to those of their respective C-terminal amphibian homologs BB and ranatensin (RT). The 4 peptides transiently increased potential difference and short-circuit current (Isc) in jejunal mucosal sheets after their serosal administration in subnanomolar concentrations with an order of potency: GRP approximately RT greater than or equal to NMB greater than BB. BB and RT were more effective in elevating Isc than GRP and NMB; all peptides had variable effects on tissue conductance. Mucosal Isc responses to GRP (1 nM) were due in part to a stimulation of net Cl- secretion. GRP-induced Isc increases were halved by serosal furosemide (0.3 mM) and reduced by 65% and 90% in tissue bathing solutions lacking Cl- or Cl- and HCO3-, respectively. Tetrodotoxin reduced Isc responses to the peptide by 40%; GRP activity remained unaffected after blockade of gut muscarinic or nicotinic cholinergic receptors by atropine or hexamethonium, respectively. These results suggest that GRP and its natural homologs stimulate active electrogenic Cl- secretion in the porcine jejunum through interactions with GRP receptors located in the intestinal mucosa and submucosa.

Amphibians↗
PubMed1991

Endothelin: a potent stimulator of intestinal ion secretion in vitro.

Effects of endothelin (ET) on electrical properties and Na+ and Cl- fluxes in stripped rabbit ileal mucosa were investigated in vitro in Ussing chambers. Results demonstrate that serosal addition of ET-1, ET-2, ET-3 or the precursor 38 amino acid 'big endothelin' produce dose-dependent increases in short-circuit current (Isc) with maximal effects at approx. 100 nM, 100 nM, 10 nM and 100 nM, respectively and half-maximal effects at 1.4 nM, 5 nM, 1.4 nM and 20 nM, respectively. Mucosal addition of ET-3 failed to elicit a response. Changes in Isc elicited by ET-3 are accompanied by decreases in net fluxes of both Na+ and Cl-. The cyclooxygenase inhibitors, indomethacin and piroxicam, inhibited the increase in Isc produced by ET-3 and indomethacin also abolished the changes in Na+ and Cl- fluxes produced by ET-3. However, no changes in the release of PGE2, thromboxane B2 or 6-keto-prostaglandin F1 alpha could be detected up to 20 min after the addition of ET-3. Preincubation of tissues with neuronal agonists or antagonists, antihistamines or an LTD4/LTE4 receptor antagonist, SKF 104353, failed to alter the response to ET-3. Furthermore, removal of serosal Ca2+ also failed to inhibit the change in Isc produced by ET-3. These results indicate that endothelin is a potent intestinal secretagogue which does not appear to elicit its response through stimulation of PGE2, thromboxane A2 or prostacyclin.

Animals↗