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Biomedical subjects

L L Shanbour

Publications and source records attributed to L L Shanbour.

At least 19 recordsLinked to original sources
PubMed1985

Failure of 16,16-dimethyl PGE2 to prevent inhibitory effect of ethanol on sodium transport in canine gastric mucosa.

By use of an in vitro canine gastric mucosal preparation, we evaluated the effects of ethanol (2, 4, 6, and 8%, vol/vol) and indomethacin (2.2 X 10(-4)M), with and without 16,16-dimethyl PGE2 pretreatment, on net sodium transport (JNanet) (mucosal to serosal) across gastric epithelium. Although administration of 2 or 4% ethanol to the mucosal bathing solution had no appreciable inhibitory effects on sodium transport, 6 and 8% ethanol and indomethacin significantly inhibited JNanet when compared with untreated control mucosa. This effect was accompanied by inhibition of transmucosal potential difference (PD) and short-circuit current (Isc). In other mucosae exposed to dimethyl PGE2 (8 X 10(-6) M) in the serosal bathing solution, significant increases in JNanet, PD, and Isc were noted when compared with control mucosa. Addition of 6 or 8% ethanol to the mucosal solution of dimethyl PGE2-pretreated tissue resulted in significant decreases in PD, Isc, and JNanet below control values that were not significantly different from mucosa exposed to 6 and 8% ethanol without PG pretreatment. When indomethacin was added to the mucosal solution following dimethyl PGE2 pretreatment, only slight decreases in PD and Isc below control levels were observed, and the inhibitory effects on JNanet induced by indomethacin without such treatment were abolished. These findings suggest that stimulation of JNanet by prostaglandin may play a role in its ability to prevent indomethacin damage to gastric epithelium but does not appear to be of importance in mediating protection against ethanol damage.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Nonprotein sulfhydryl compounds in canine gastric mucosa: effects of PGE2 and ethanol.

By use of an in vivo canine chambered stomach preparation in which the gastric mucosa was partitioned into two equal halves, the effect of topical 16,16-dimethyl PGE2 (DMPGE2) (1 microgram/ml of perfusate) and 8% and 40% ethanol on tissue levels of nonprotein sulfhydryl compounds was assessed. Both DMPGE2 and 8% ethanol significantly increased (P less than 0.005) mucosal levels of nonprotein sulfhydryls when compared with corresponding mucosa bathed with saline alone. In contrast, mucosa bathed with 40% ethanol showed significantly decreased levels. If mucosa was bathed with DMPGE2 or 8% ethanol prior to exposing the stomach to 40% ethanol, this depletion in sulfhydryl compounds was not observed. Since other experimental observations have shown that exogenously administered prostaglandins and mild irritants (such as low-dose alcohol) can prevent gastric mucosal damage by necrotizing agents (such as high-dose alcohol), our findings are consistent with the hypothesis that nonprotein sulfhydryls may play a role in mediating gastric mucosal protection.

16,16-Dimethylprostaglandin E2↗
PubMed1984

Prevention of the inhibitory effects of aspirin on sodium transport in canine gastric mucosa by prostaglandin. Correlation with mucosal morphology.

Using an in vitro canine gastric mucosal preparation, this study evaluated the effects of 1 mM aspirin in a buffered Ringer solution (pH = 7.4), with and without concomitant prostaglandin (PG) treatment, on net sodium transport (mucosa to serosa) across gastric epithelium. Administration of aspirin to the mucosal bathing solution for 2 hr significantly decreased the potential difference (PD), short circuit current (Isc), and net sodium transport (net J-Na+) when compared with untreated control mucosa. In mucosa treated with 16,16-dimethyl PGE2 (8 X 10(-6) M) in the serosal bathing solution 40 min after aspirin exposure and for 80 min thereafter, the initial inhibitory effects on PD, Isc, and net J-Na+ induced by aspirin were completely reversed within 40 min of PG treatment, having returned to control values. Histologically, mucosa exposed to aspirin alone showed evidence of diffuse cellular injury involving 50-60% of the surface epithelium. In contrast, mucosa treated with prostaglandin in conjunction with aspirin exposure demonstrated damage involving only 20-30% of the epithelium. These findings suggest that stimulation of sodium transport by PG may play a role in mediating the cytoprotective effects of PGs against aspirin-induced gastric mucosal injury.

Animals↗
PubMed1984

Sodium transport in Rana pipiens gastric mucosa.

The transport properties of frog gastric mucosa in vitro have been reexamined in conditions analogous to those used in studies on mammalian systems in which net movements of sodium were observed. Net transport of sodium across frog gastric mucosa was not observed to occur when the mucosal surface was bathed with a well-buffered solution of near neutral pH, indicating that failure to demonstrate sodium transport across frog stomach in previous work could not be ascribed to the low pH value of the solution usually used as the mucosal fluid. Addition of 5 X 10(-4) M amphotericin B to the mucosal solution elicited net transport of sodium and an increase in short-circuit current. These findings indicate that sodium transport may contribute to the electrolyte physiology of frog gastric mucosa in some experimental conditions, and may limit the utility of the three-variable model proposed by Hogben.

Amphotericin B↗
PubMed1983

Inhibition of active sodium transport by cytochalasin B in rat jejunum in vitro.

The effects of cytochalasin B on electrophysiological properties and sodium transport in rat jejunum in vitro are described. Stripped paired rat jejunal segments were maintained in Ussing chambers with Leibovitz's (L-15) tissue culture medium bubbled with 100% oxygen. L-15 medium contains galactose as the only sugar, and an assortment of amino acids and cofactors to nourish the tissue. Electrophysiological parameters of short-circuit current (Isc) and transepithelial potential difference could be maintained for up to 4 h in control tissues. Upon application of cytochalasin B (20 micrograms/ml), on the mucosal side, Isc and potential difference fell within 1 h from 1.93 +/- 0.12 to 1.09 +/- 0.14 (mean +/- S.E.) muequiv./cm2 per h and from 5 to 2.5 mV. Tissue resistance remained unchanged at approx. 110 omega X cm2 for up to 4 h. 22Na net flux was 4.1 +/- 0.9 muequiv./cm2 per h during the last control period and fell to zero within 1 h after cytochalasin B treatment. Transmission electron micrographs revealed no gross morphological changes at this dose. Absorptive junctional morphology was apparently not altered by cytochalasin B treatment, a finding which was consistent with the stable transepithelial electrical resistance observed during exposure to this drug. Active sodium transport processes coupled to hexose, amino acid, and chloride movements are all possible in L-15 medium. However, following exposure to 20 micrograms/ml cytochalasin B, all net sodium transport is completely inhibited. The data are consistent with the hypothesis of a common regulator for active sodium transport processes which is modulated through structural changes in cytoskeletal organization.

Animals↗
PubMed1983

Effects of 16,16-dimethyl prostaglandin E2 on alkaline secretion in isolated canine gastric mucosa.

An isolated fundic mucosal preparation of dog stomach which is capable of exhibiting an alkaline secretion is described. A stable secretion was established 40 min to 1 hr after the mucosa was pretreated with the H2-antagonist cimetidine to block spontaneous acid output. Alkaline secretion decreased when Ca2+ was removed from the nutrient solution. This secretion was stimulated by dibutyryl cyclic GMP, but was not altered by acetylcholine, carbachol, or 16,16-dimethyl PGE2. Alkaline secretion from a similar antral mucosal preparation was stimulated by 16,16-dimethyl PGE2. We conclude that the 16,16-dimethyl PGE2-stimulated bicarbonate secretion previously demonstrated in in vivo canine fundic mucosa is not the result of a direct effect of PG on gastric mucosal cells and that an intact blood circulation or cholinergic innervation is required for this action to occur.

16,16-Dimethylprostaglandin E2↗
PubMed1983

Route of ethanol administration and gastric acid output during chronic conditions.

The effect of intravenous or intragastric ethanol on gastric secretion was determined in chronic ethanol-fed and matched control rats. In vivo, basal and histamine-stimulated acid outputs were inhibited by acute intragastric ethanol to a greater extent in chronic control rats than in ethanol-fed rats. In contrast, intravenous ethanol stimulated basal and potentiated histamine (H)-stimulated acid output (blocked by cimetidine but not atropine) in ethanol-fed rats but not in chronic control rats. Serum gastrin levels were not significantly altered by ethanol. In vitro, mucosal ethanol inhibited basal and H-stimulated acid secretion by mucosae from chronic control and ethanol-fed rats, but serosal ethanol did not significantly alter acid secretion. In conclusion, chronic ethanol intake results in higher acid outputs following acute exposure to intravenous or intragastric ethanol or in vitro exposure to mucosal ethanol as compared to studies using matched control rats.

Animals↗
PubMed1982

Acute effect of ethanol on metabolite concentrations of dog pancreas in vivo.

Sections of dog pancreas were freeze-clamped before and 1 hr after oral administration of 1 g/kg of ethanol in anesthetized, respirated, 24-hr-fasted animals, and multiple metabolites were determined in the perchloric acid extract of the frozen tissue. In spite of the fact that the pancreas contained little or no alcohol dehydrogenase activity (less than 0.01 IU/g of tissue), significant metabolite changes did occur. Although arterial oxygenation was constant and adequate (pO2 = 100 +/- 7 mM Hg) there was a significant 1.7-fold rise in L-lactate and fall in the cytoplasmic free [NAD+]/[NADH] ratio from 719 +/- 87 to 453 +/- 88 after ethanol. Except for a tendency for L-malate and L-alpha-glycerolphosphate to parallel the rise in L-lactate, there was little consistent disturbance in the remainder of the glycolytic metabolites (glucose, glucose 6-phosphate, pyruvate, 2-ketoglutarate, citrate, 3-phosphoglycerate, etc.) or in high energy intermediates and related compounds (ATP, creatine phosphate, ADP, Pi, creatine). There was, however, an unexpected and significant fall in the levels of the major transaminating amino acids, L-glutamate, L-aspartate, and L-alanine. The results can be only partially explained by an influence of blood-borne metabolites and imply significant effects of ethanol on the metabolism of the pancreas in vivo not directly mediated through alcohol dehydrogenase. Evidence is presented suggesting that both L-alanine and L-aspartate aminotransferases are functioning near equilibrium in the pancreas in vivo.

Amino Acids↗
PubMed1981

Transport in mammalian gastric mucosa.

Experiments in mammalian gastric mucosae lead to the following conclusions: 1. Sodium, potassium, and chloride are all required in the serosal solution but not on the mucosal side for acid secretion to occur. The only exception to this is in the dog, for which Cl- is required on both sides. 2. Most mammalian gastric mucosa actively absorb Na+. This 2. Most mammalian gastric mucosa actively absorb Na+. This absorption can be blocked by amiloride in the mucosal solution or by ouabain on the serosal side. The Na+ absorption probably occurs in some cell type other than parital cells. 3. Sodium and chloride move through separate transport pathways across the serosal border. 4. Hydrogen and chloride secretion are closely linked; however the secretion does not appear to be in the neutral HCl form. 5. There is a ouabain-sensitive Na+-K+ pump at the serosal membrane. 6. An increase in intracellular cAMP can initiate acid secretion. In addition cAMP appears to play a role physiologically at least in the initiation of histamine-stimulated acid secretion.

Acetylcholine↗
PubMed1980

Direct effect of ethanol on acid secretion in isolated canine gastric mucosa.

The direct effects of ethanol on resting and secreting (histamine = H, pentagastrin = G, and acetylcholine = A) gastric mucosa were determined using an in vitro chamber preparation. Ethanol (E) produced no effect on acid (H+) secretion during resting conditions but concentrations above 2% (4% and 8%) decreased electrical potential difference (PD), short-circuit current (Isc) and resistance (R). With H-induced H+ secretion, E at 8% on mucosal side decreased H+ secretion (4.11 +/- 0.34 to 0.64 +/- 0.45 microEq/cm2hr), Pd (32 +/- 2 to 4.9 +/- 0.6 mV), Isc (5.0 +/- 0.3 to 1.1 +/- 0.1 microEq/cm2hr), and R (237 +/- 15 to 174 +/- 68 hm . cm2). Washout of E produced recovery in all parameters. With P-induced H+ secretion, E decreased H+ secretion (1.63 +/- 0.11 to 0.51 +/- 0.18), PD (42 +/- 5 to 13 +/- 3), Isc (5.71 +/- 0.38 to 2.22 +/- 0.45), and R (274 +/- 21 to 218 +/- 13). With A-induced H+ secretion, E decreased H+ secretion (1.16 +/- 0.06 to 0.45 +/- 0.23), PD (38 +/- 1 to 12 +/- 1), Isc (5.69 +/- 0.40 to 1.94 +/- 0.09) and R (253 +/- 22 to 226 +/- 22). When E was placed on the serosal side, 10% was necessary to inhibit H+ secretion and all the electrical parameters increased. Hypertonic sucrose (695.6 mM in mucosal side) produced an immediate decrease in H+ secretion, PD and Isc but increased R. These data indicate that the direct action of E is not to stimulate but rather to inhibit secretagogue-induced gastric H+ secretion.

Acetylcholine↗
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↗
PubMed1979

Chloride, sodium, potassium and hydrogen ion transport in isolated canine gastric mucosa.

1. The fluxes of isotopically labelled Na+, Cl- and K+ in each direction and H+ secretion across isolated dog gastric mucosa were measured under short-circuit conditions. 2. In the non-stimulated state, the net flux of Na+ was 6.61 micronequiv/cm2.hr from mucosal (luminal, secretory) to serosal (nutrient, blood) side, whereas the net flux of Cl- was only 0.79 micronequiv/cm2.hr, and the direction was from serosal to mucosal side. 3. There was a positive correlation between the net flux of Cl- and acid secretion, however, net flux of Na+ was not correlated with acid secretion initiated by secretagogue treatment. 4. With ion substitution studies, only replacement of mucosal Na+ with choline produced a highly significant decrease in potential difference (p.d.). This indicates that active transport of Na+ from the mucosal to the serosal side is the most important source for the generation of the gastric p.d. in dog gastric mucosa. 5. From ion substitution studies, it was also observed that Cl- in either mucosal or serosal solution is necessary for maintaining acid secretion; whereas only serosal Na+ and K+ are essential for acid secretion. Removal of either Na+ or K+ from the mucosal solution had no effect on acid secretion. 6. Substitution of SO2-(4) for Cl- had no effect on active transport of Na+, but choline substitution for Na+ diminished active transport of Cl-.

Animals↗
PubMed1978

Effects of ethanol on sodium, 3-O-methyl glucose, and L-alanine transport in the jejunum.

Effects of ethanol on Na+, Cl-, 3-O-methyl glucose (3-O-MG), and L-alanine fluxes were studied in the isolated rattit jejunal mucosa. Ethanol (3% v/v present on both sides of the mucosa) decreased electrical potential difference (PD), short-circuit current (Isc) and inhibited active transport of Na+, 3-O-MG, and L-alanine. This concentration also increased the permeability of the mucosa for Cl-, 3-O-MG, and L-alanine. Ethanol at 5.4% potentiated the effects on PD, Isc, and the permeability for electrolytes and organic substances. These effects of ethanol could not be fully explained by an osmotic action.

Alanine↗
PubMed1978

Acid secretion by isolated canine gastric mucosa.

1. An isolated gastric mucosal preparation from the dog stomach which is capable of acid secretion is described. Average values for normal resting potential difference (p.d.) was 49 +/- 2 mV (mucosal side negative with respect to the serosal side), short-circuit current (Isc) was 172 +/- 4 muA and resistance (R) was 285 +/- 6 omega.cm2. Low rates of spontaneous acid secretion (0-0.58 muequiv/cm2.hr) were present initially but following short-circuiting of the tissue these values decreased to low levels (less than 0.1 muequiv/cm2.hr) within an hour. 2. Histamine in doses exceeding 10(-6)M stimulated acid secretion, increased Isc and decreased R. Concentrations ranging from 10(-5) to 8 X 10(-4)M produced maximal secretion. The maximal secretory rate achieved was 4.24 +/- 0.35 muequiv/cm2.hr. 3. Pentagastrin (10(-8)M) and acetylcholine (10(-6)--10(-5)M) also stimulated acid secretion with a lower maximal secretion as compared to histamine stimulation. These concentrations of pentagastrin and acetylcholine did not alter histamine stimulated acid secretion. Higher concentrations of pentagastrin (10(-6)M) and acetylcholine (10(-4) M) reversibly inhibited acid secretion of histamine stimulated mucosa. 4. These results demonstrate that there are many similarities between in vitro and in vivo findings on the dog stomach, indicating the great potential of the in vitro dog gastric mucosa for studies on the mechanism of action and interaction of gastric secretagogues.

Acetylcholine↗
PubMed1977

Acute effects of N-methyl-N'-nitro-N-nitrosoguanidine on canine gastric mucosa.

The electrophysiological effects of the chemical gastric carcinogen N-methyl-N'-nitro-N-nitrosoquanidine (MNNG) were determined in an in vivo chambered canine stomach and in an in vitro canine gastric mucosal preparation. In the in vivo stomach, the topical application of 2.5 mg MNNG/ml decreased the transmural electrical potential difference, and the systemic blood pressure was essentially unchanged. In the in vitro preparation, exposure of the mucosal side of the isolated canine gastric mucosa to 0.25 and 2.5 mg MNNG/ml for 1 hour sequentially or exposure of the serosal side to 2.5 mg MNNG/ml for 2 hours inhibited net Na+ and Cl- fluxes. With longer duration, the undirectional fluxes of Na+ and Cl- increased, indicating an increase in permeability. These findings suggested that inhibition of active transport in the gastric mucosa may have an important function in the gastric carcinogenicity of MNNG.

Animals↗