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Biomedical subjects

W Silen

Publications and source records attributed to W Silen.

At least 145 records · Page 8Linked to original sources
PubMed1978

Effect of the acid secretory state on intramural pH of rabbit gastric mucosa.

Intramural pH of the gastric mucosa was measured using a microelectrode technique in rabbit gastric pouches under different secretory conditions and luminal acidity. Exposure of spontaneously secreting or metiamide-treated fundic pouches to a relatively high concentration of luminal acid. HCl 120 mM, for 60 min, led to a marked net loss of luminal H+ which was associated with a significant decrease in the intramural pH (7.28 +/- 0.09 to 6.88 +/- 0.10 and 7.23 +/- 0.07 to 6.99 +/- 0.09, respectively). A linear relationship was observed between the rates of net disappearance of luminal acid and the intramural pH. All 10 spontaneously secreting and five metiamide-treated pouches had superficial mucosal erosions. In contrast, when fundic pouches were exposed to luminal acid in histamine-treated animals, the net loss of luminal H+ was negligible and the intramural pH remained at its base-line level (7.25 +/- 0.07). Histamine stimulation without acid in the lumen caused a small but insignificant increase in the intramural pH (7.27 +/- 0.03 to 7.39 +/- 0.05). Only three of the eight histamine-treated fundic pouches had lesions. In the antral pouches the intramural pH changes in response to exposure to luminal acid were smaller and histamine treatment did not influence the intramural pH. None of the antral pouches had lesions. The results suggest that acidification of the tissue by the diffusion of luminal acid may be an important factor in the pathogenesis of acute gastric ulceration. The acid secretory state of the gastric mucosa can significantly influence the acid-base balance in the mucosa and thus modify its response to acid diffusing from the lumen. Histamine stimulation protected the gastric mucosa by improving its buffering capacity and/or otherwise decreasing the diffusion of H+ from the lumen into the mucosa.

Animals↗
PubMed1978

Effects of lysolecithin on isolated gastric mucosa.

The effects of lysolecithin, a normal constituent of duodenal juice, on gastric mucosa were measured under isolated conditions. In a relatively low concentration (0.5 mg/ml), lysolecithin, added to the luminal side, caused liberation of organic acids without altering the spontaneous rate of mineral (i.e., HCl) acid secretion by fundic mucosa. The low concentration of lysolecithin also did not appear to affect other active ion transport processes or permeability of either fundic or antral mucosa. However, at a higher concentration (1 mg/ml) lysolecithin inhibited spontaneous mineral acid secretion by fundus, altered active transport of other ions, and increased mucosal permeability of both fundic and antral mucosa. The results suggest that intraluminal lysolecithin in concentrations found in vivo may contribute to gastric mucosal damage.

Animals↗
PubMed1977

Secretory state of gastric mucosa and resistance to injury by exogenous acid.

The capacity of the stomach to resist the effects of highly acid solutions was assessed by comparing the effects of such solutions on spontaneously secreting, stimulated, and inhibited gastric mucosae of rabbits in vivo and frogs in vitro. Exposure of unstimulated resting mucosa to HC1, 120 mM, for 60 minutes produced superficial erosions in all rabbits, whereas such lesions were observed in only one of ten animals stimulated with histamine. Metiamide obviated the protective effect of histamine against ulcerations even though it did not reduce H+ secretion to zero. Exposure of inhibited isolated frog fundic mucosa to HC1 resulted in significant deterioration of electrical parameters, suggesting impairment of active transport processes and increased tissue permeability. These data are consistent with the hypothesis that actively secreting gastric mucosae from two species resist injury to exogenous acid more effectively than do resting or inhibited tissues, perhaps in part as a result of a greater alkaline tide.

Animals↗
PubMed1977

Distribution of carbonic anhydrase within the gastric mucosa.

Bullfrog fundic mucosa was separated into fractions containing predominantly surface epithelial cells, mucous neck cells, and and oxyntic cells, respectively, and the carbonic anhydrase concentration of each fraction and of antral mucosa was measured. There were no significant differences between the enzyme concentrations of these fractions. The mean level was 12.4 units of activity per milligram of protein. The cellular localization of carbonic anhydrase in the gastric fundic and antral mucosa of the bullfrog, rat, rabbit, and dog was studied using a specific histochemical technique. The enzyme was shown to be present in both parietal and nonparietal epithelium of all species and to characterize a specific cell type in the dog antrum. The widespread distribution of high levels of carbonic anhydrase activity in both acid secreting and nonsecreting cells of the gastric mucosa suggests a possible role for the enzyme beyond one solely relating to acid secretion.

Animals↗
PubMed1976

Influence of acid secretory state on the gastric mucosal tolerance to back diffusion of H+.

The effect of back diffusion of H+ PON THE POTENTIAL DIFFERence (PD), electrical resistance (R), and short circuit current (Isc) of spontaneously secreting and burimamide-inhibited amphibian gastric mucosae were studied in vitro. When back diffusion of H+ was induced by the passage of an electrical current of 510 mua per cm2 from the secretory (S) side of pH 2.25 to the nutrient side (N) for 30 min, the spontaneously secreting mucosae showed small decreases in PD (23.6 leads to 16.2 mv) and Isc (80 leads to 61 mua per cm2) but no significant change in R. In the burimamide-inhibited mucosae there were marked and significantly greater decreases of PD (26.8 leads to 3.4 mv), R (473 leads to 170 ohms cm2) and Isc (50 leads to 13 mua per cm2). When back diffusion of H+ was induced by establishing a concentration gradient of H+ from S leads to N or by exposing the secretory surface to sodium taurocholate with secretory pH 2.25, the burimamide-inhibited tissue demonstrated significantly greater depression of the electrical parameters than the secreting mucosae. Intracellular pH, measured by the 5,5-dimethoxyazolidine-2,4-dione method, was significantly higher in the histamine-stimulated tissues (7.28) than in the metiamide-inhibited tissues (7.11). These studies strongly suggest that the secretory status of the mucosa and hence its acid-base status are important determinants in the tolerance of the tissue to exogenous back diffusion of H+. The measure of absolute loss of H+ From the mucosal solution alone may not be an adequate assessment of the gastric mucosal barrier.

Animals↗
PubMed1975

Mechanisms of acid disposal in canine duodenum.

Distal duodenal pouches chronically excluded from the intestinal stream were perfused in seven awake dogs by a constant-circulation technique using isomolar solutions containing 60-120 mM HCl. The rate of disappearance of hydrogen ions (H+) and net ion movements was measured. In all experiments there was a loss of H+ from the perfusate accompanied by a gain of sodium (Na+), potassium (K+) and chloride (Cl-), together with an increase in volume and a decrease in osmolality. The magnitude of this H+ loss was a function of instillate [H+]. The H+ lost by neutralization was separated from that lost by diffusion by calculations based on the assumption that the observed changes in somolality were the result of neutralization by bicarbonate (HCO3-). The bulk of the acid (67%) was lost by neutralization, the remainder back-diffusing in a one-to-one exchange for diffusable Na+. This ability to dispose of acid decreased with increasing age of the pouches due to a diminished volume of HCO3- secretion, the magnitude lost by backdiffusion remaining unchanged.

Animals↗
PubMed1975

Effects of bile salts on amphibian gastric mucosa.

The effect of five different bile salts on the mucosal or serosal surface of isolated bullfrog gastric mucosa was investigated. Serosal exposure (30 min) to 15-40 mM taurocholate (TCA) or taurodeoxycholate (TDCA), 10-40 mM deoxycholate (DCA), or 2.5-7.5 mM cholate (CA) typically produced a marked increase in resistance (R) and a decrease in potential difference (PD), short-circuit current (I-sc), and H+ secretion. Flux of 36Cl from serosal to mucosal solution decreased progressively. The flux of [14C]sucrose across the mucosa was slightly decreased. Microscopy showed condensation of the parietal cells. Mucosal exposure (30 min) at concentrations above 2.5 mM DCA or CA and 15 mM TCA and TDCA caused a marked decrease in R, PD, I-sc, and H+ secretion, and the flux of [14C]sucrose across the mucosa was increased. Extreme destruction of the surface mucous cells was the primary histologic finding. The effect of dehydrocholate was identical to that of TCA. Mucosal bile salts cause an increased permeability primarily by injury of the surface epithelium whereas serosal bile salts affected primarily the oxyntic cells.

Animals↗
PubMed1975

Acid-base balance in amphibian gastric mucosa.

It has been established that H+ secretion can be maintained in frog stomach in the absence of exogenous CO2 by using a nutrient bathing fluid containing 25 mM H2PO4 (pH approximately equal to 4.5) or by lowering the pH of a nonbuffered nutrient solution to about 3.0-3.6. Exogenous CO2 in the presence of these nutrient solutions uniformly caused a marked decrease in H+ secretion, PD, adn short-circuit current (Isc) and an increase in transmucosal resistance (R). Elevation of nutrient [k+] to 83 mM reduced R significantly but transiently without change in H+ when nutrient pH less than 5.0, whereas R returned to base line and H+ increased when nutrient pH greater than 5.0. Acidification of the nutrient medium in the presence of exogenous CO2 results in inhibition of the secretory pump, probably by decreasing intracellular pH, and also interferes with conductance at the nutrient membrane. Removal of exogenous CO2 from standard bicarbonate nutrient solution reduced by 50% the H+, PD, and Isc without change in R; K+-free nutrient solutions reverse these changes in Isc and PD but not in H+. The dropping PD and rising R induced by K+-free nutrient solutions in 5% CO2 - 95% O2 are returned toward normal by 100% O2. Our findings support an important role for exogenous CO2 in maintaining normal acid-base balance in frog mucosa by acting as an acidifying agent.

Acid-Base Equilibrium↗
PubMed1975

Mechanisms of disposal of acid and alkali in rabbit duodenum.

Stripped duodenal mucosa of rabbits was mounted in Ussing chambers containing a Ringer solution gassed with 100% O2. The disappearance of acid or alkali from the mucosal solution of short-circuited tissue was measured with a pH stat while the serosal pH was kept at 7.4. The duodenum rapidly disposed of both acid and alkali; neither property was altered by gassing with N2 while iodoacetate was in the perfusing solutions. Prevention of release of CO2 from the mucosal chamber obliterated the early rapid phase of acid disposal by the mucosa while a similar maneuver in the serosal chamber increased the appearance of serosal acid without altering the rate of acid disposal. Gut sacs of rabbit duodenum in vitro and in vivo showed a positive correlation between acid disposal and the rate of luminal CO2 production. While acid disposal progressively decreased with time for the in vitro gut sacs, the in vivo gut sac showed no fatigue in this respect. Luminal acidification in the Ussing chamber was associated with a profound reduction in short-circuit current (Isc), partially reversible by elevation of the mucosal pH but not by luminal glucose. Our data suggest that acid disposal occurs in part by intraluminal neutralization and in part by diffusion into the mucosa.

Acid-Base Equilibrium↗