Yuh-Jyh Kuo

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

Effects of ethanol on Na+, Cl−, 3-O-methyl glucose (3-O-MG), andl-alanine fluxes were studied in the isolated rabbit 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, andl-alanine. This concentration also increased the permeability of the mucosa for Cl−, 3-O-MG, andl-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.

Electrophysiological Effects of Burimamide and 16,16-Dimethyl Prostaglandin E2 on The Canine Gastric Mucosa

The electrophysiological effects of two potent inhibitors of gastric acid secretion, burimamide and 16,16-dimethyl prostaglandin E2 (dm-PGE2), were determined in an in vivo histamine-stimulated canine stomach preparation and an in vitro canine gastric mucosal preparation. In the in vivo stomach preparation, intravenous burimamide caused a decrease in acid secretion, an increase in transmucosal potential difference (PD) and the relative resistance (R) was essentially unchanged. Intravenous dm-PGE2 also inhibited acid secretion and increased PD but, in contrast to burimamide, increased R. In the in vitro preparation, the unidirectional flux of sodium from mucosa to serosa increased after dm-PGE2 but not after burimamide. Passive sodium fluxes and unidirectional chloride fluxes were not altered after either agent. These findings suggest that increased active transport of sodium from mucosa to serosa is at least partially responsible for the observed increase in transmural PD with dm-PGE2, an agent which also decreases hydrogen ion transport. With burimamide the increased PD was due primarily to inhibition of hydrogen ion secretion.

Effect of ethanol on permeability and ion transport in the isolated dog stomach

Effects of ethanol on permeability and ion transport in the isolated dog gastric mucosa were studied. The unidirectional fluxes of urea and sodium were increased slightly in 3% (v/v) ethanol and markedly in 20% (v/v) ethanol, but those of chloride only increased in 20% ethanol. The increase in the unidirectional fluxes of electrolytes in 20% ethanol was associated with increased ionic conductance (decreased resistance). Measured as net ionic flux at zero electrochemical potential difference, the active transport of chloride, sodium and hydrogen ions was inhibited by 20% ethanol. Sodium ion and hydrogen ion transport were also inhibited after 5 minutes in 3% ethanol. We conclude that ethanol increases permeability and inhibits ion transport in the isolated dog gastric mucosa.

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 inin 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.

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.

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 Leibovitzs (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.

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 signifcantly alter acid secretion. In conclusion, chronic ethanol intake results in higher acid outputs following acute exposure to intravenous or intragastric ethanol orin vitro exposure to mucosal ethanol as compared to studies using matched control rats.

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.