Search PubMed⌕ Search

Biomedical subjects

W Silen

Publications and source records attributed to W Silen.

At least 127 records · Page 7Linked to original sources
PubMed1980

Effect of bile salts and related compounds on isolated esophageal mucosa.

The effect of several potentially harmful agents in gastric juice and duodenal contents on esophageal mucosa was investigated in the presence or absence of luminal H+ using an in vitro technique. Isolated rabbit esophageal mucosae were incubated in an Ussing chamber, and during exposure to the test agents mucosal integrity was assessed by measurement of mucosal potential difference (PD), tissue electrical resistance (R), and when luminal acid was present, the tissue permeability to H+. At pH 3.5 taurocholate caused a marked decrease in the PD and R and a substantial increase in the rate of luminal H+ loss. This effect was dependent on the presence of luminal H+, since no changes were observed with taurocholate at pH 7.4. In contrast, two of the three deconjugated bile salts tested at pH 7.4, deoxycholate and chenodeoxycholate, caused a profound reduction in the PD and R, similar to that observed with taurocholate in the presence of H+. Pepsin in the presence of H+, lysolecithin to a lesser degree, and trypsin in the absence of H+ also adversely affected isolated esophageal mucosa, but the effects were less pronounced than those caused by bile salts. Our data suggest that different mechanisms are operative in the pathogenesis of acidic and alkaline reflux esophagitis. In the presence of gastric H+, pepsin, and conjugated bile salts are the substances responsible for the greatest injury. In contrast, when acid is absent, trypsin and especially deconjugated bile salts are more crucial pathogenetic factors.

Animals↗
PubMed1980

Effect of 16-16-dimethyl-prostaglandin E2 on ulceration of isolated amphibian gastric mucosa.

In order to investigate the cytoprotective action of 16-16-dimethyl-prostaglandin E2 (16-16D), we studied its effect on sacs of isolated amphibian gastric mucosa known to ulcerate with high frequency in the absence of nutrient HCO3-. The actions of 16-16D, 2.85 X 10(-6) M, were also studied in an in vitro chamber. The incidence of ulceration in HCO3- -free nutrient media containing 10(-4) M histamine was significantly reduced by 16-16D. When artificial gastric juice (AGJ) was instilled into the lumen of the sac, protection occurred only after a pretreatment period of 60 min. Cytoprotection was not observed when active secretion of H+ was inhibited with 10(-3) M metiamide, and AGJ was placed in the lumen of the sac. In open sheets of fundus stimulated with 10(-4) M histamine, 16-16D did not influence H+ secretion. Isc was significantly higher than in control tissues. We conclude that 16-16D is cytoprotective in amphibian gastric mucosa by an action independent of changes in acid secretion or in blood flow. In addition, our studies suggest that 16-16D may increase the availability to the surface cells of nutrient HCO3- produced by actively secreting oxyntic cells.

16,16-Dimethylprostaglandin E2↗
PubMed1979

Effects of vagotomy with and without pyloroplasty on weight and food intake in rats.

Bilateral truncal vagotomy performed in 13 rats reduced weight gain by 26% compared to controls, but also produced gastric distension. Addition of pyloroplasty was found to facilitate gastric drainage in vagotomized rats, and both procedures were then performed in 57 rats of both sexes and varying initial weights. When fed ad libitum, vagotomized animals maintained a weight 14-30% less than controls over periods of 30-300 days. When pair fed, normal rats and rats with vagotomy and pyloroplasty weighed the same. Various partial vagotomies had no effect on weight gain. It was concluded that vagotomy reduces weight gain in rats, that the reduction is the result of decreased food intake, and that the effect of vagotomy is probably not due to gastric distension.

Animals↗
PubMed1978

Antacid titration in the prevention of acute gastrointestinal bleeding: a controlled, randomized trial in 100 critically ill patients.

We randomized 100 critically ill patients at risk of developing acute gastrointestinal ulceration and bleeding into two groups. One (51 patients) received antacid prophylaxis, and the other (49 patients) received no specific form of prophylaxis. Hourly antacid titration kept the pH of the gastric contents above 3.5. Two of the 51 patients who received antacid prophylaxis and gastrointestinal bleeding. Twelve of the 49 control patients bled (P less than 0.005). Of the 12 patients in the control group who bled, seven were placed on antacid medication, and all seven apparently stopped bleeding. Analysis of all the patients showed that an increasing prevalence of respiratory, failure, sepsis, peritonitis, jaundice, renal failure and hypotension was correlated with a greater frequency of bleeding. No patients required operative treatment to control bleeding. These data indicate that the occurrence of acute gastrointestinal bleeding in critically ill patients can be reduced by antacid titration.

Acute Disease↗
PubMed1978

Anastomotic dehiscence after low anterior resection of the rectum.

Thirty-two patients who had anastomoses to the extraperitoneal rectum underwent radiographic contrast studies about two weeks after operation in order to determine the incidence of anastomotic dehiscence. No extravasation occurred in the sixteen anastomoses in which the middle hemorrhoidal arteries were intact, but partial disruption occurred in four of seventeen (24%) anastomoses in which the middle hemorrhoidal arteries were sacrificed. Since not all patients with anastomotic dehiscence after low anterior resection are symptomatic, the incidence of anastomotic breakdown will be under-estimated unless x-ray studies are performed. More data are required for a better understanding of the technical features of operation which will reduce the incidence of leakage from anastomoses to the extraperitoneal rectum.

Adult↗
PubMed1978

Bacterial contamination of the biliary tree after choledochostomy.

Secondary exogenous contamination of bile after choledochostomy could be an important cause of long-term morbidity if infection persists after removal of the T tube. Surprisingly, documentation of the frequency of conversion of sterile to infected bile after choledochostomy has rarely been recorded. Patients undergoing exploration and T-tube drainage of the common bile duct between July 1966 and January 1975, in whom intraoperative and postoperative cultures of bile were available, were studied. Postoperative cultures were obtained from five to forty days after operation. Of ninety-five patients available for study, contamination developed postoperatively in previously sterile bile in 44 per cent. The common duct bile contained bacteria at operation in 42 per cent and remained sterile throughout in 14 per cent. The most common secondary contaminants were klebsiella group and Escherichia coli. The fate of the contaminating organisms in a biliary tree without anatomic abnormalities is unknown. Two cases are presented which suggest that persistent infection may linger in the biliary tree for many years and give rise to pigment calculi. Since bacterial cannot be eradicated so long as a foreign body remains in the common duct and because such bacteria may cause symptoms even in an anatomically normal biliary tree, we suggest that a closed system of biliary drainage be employed and that appropriate antibiotic therapy be instituted for seven to ten days after removal of the T tubes.

Aged↗
PubMed1978

Na+ transport by mammalian stomach.

Gastric mucosas from newborn pigs (0--20 days) and rabbits (0--20 days) were used for in vitro investigation of active Na+ transport during resting (no HCl secretion) conditions. As measured with 22Na+, these tissues actively absorb Na+ from the mucosal-to serosal (m-t-s) bathing solution during both open-circuit and short-circuit current (Is) conditions. In the nonsecreting state, net Na+ transport accounts for 40--60% of Isc. The remaining current is provided by net s-to-m flux of Cl-. Amiloride (2-5 X 10(-5) M) in the mucosal solution abolishes this active Na+ transport by inhibiting m-to-s fluxes of Na+ (JNams). In vivo-in vitro experiments showed that active Na+ transport is a normal function of the resting mammalian stomach. Decreasing pH of the mucosal solution below pH 5 reversibly causes decreased current-generating capability of the tissue. Pretreatment of the tissue with amiloride abolishes this pH effect. The implication is that the low pH affects the Na+-entry step into cells. "Titration curves" of current vs. pH had an apparent pK approximately 4.0. Ouabain and K+-free solutions both cause decreases in active Na+ and Cl- current. Calculations indicate that a shunt may account for only a small (less than 30%) percentage of total transepithelial conductance.

Amiloride↗
PubMed1978

Effects of methylprednisolone on hydrogen ion absorption in the canine stomach.

The effect of methylprednisolone (2 mg/kg per day given parenterally for 3 doses, 2 wk or 12 wk) on the permeability of mammalian gastric mucosa to hydrogen ion (H(+)) was examined with denervated fundic pouches in dogs with antrectomies. Transmucosal electric potential difference (PD) and net fluxes of H(+) and Na(+) were determined for luminal [H(+)] from 20 to 160 mM and [Na(+)] from 1 to 140 mM ([H(+)] and [Na(+)] were varied reciprocally). The PD was 50-60 mV lumen negative and was constant over the entire range of Na(+) and H(+) concentration tested. Net H(+) flux varied linearly with [H(+)]. Extrapolation indicated apparent H(+) loss at zero luminal concentration, suggesting a basal HCO(3) (-) secretion. Addition of acetylsalicylic acid (ASA) or taurocholate decreased the PD to 30-40 mV and increased threefold the slope of the relation between net H(+) flux and [H(+)] (k(H)). Calculation of PD-independent permeability constants for H(+) (P(H)) with the Goldman constant field equation indicated that this increase in k(H) could not be attributed solely to the associated decrease in PD. Prednisolone administered for 3 doses had no effect on either the basal mucosal permeability to H(+) or the altered permeability induced by ASA or taurocholate. Chronic administration induced a low rate of basal acid secretion (at 12 wk) but had no effect on either PD or k(H). However, the increase in k(H) and P(H) that developed upon addition of ASA or taurocholate in chronically treated dogs was more than one and a half times that of controls. These data suggest that prolonged treatment with glucocorticoids increases susceptibility of the gastric mucosa to damage by agents that increase permeability to H(+).

Absorption↗