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Biomedical subjects

H J Binder

Publications and source records attributed to H J Binder.

At least 127 records · Page 7Linked to original sources

Effect of histamine H2-receptor antagonists on delayed hypersensitivity.

The delayed skin-test response to four antigens was assessed before and after 6 weeks' cimetidine therapy in patients with duodenal-ulcer disease. In the eight patients who received cimetidine there was a significant increase in both erythema and induration after six weeks' cimetidine therapy. In contrast, the intensity of delayed-hypersensitivity reactions at 6 weeks was not increased in eight control patients who did not receive cimetidine. These studies indicate that therapy with an H2-receptor antagonist may be associated with an augmentation of delayed hypersensitivity responses.

Cimetidine↗

Effect of cimetidine on intrinsic factor and pepsin secretion in man.

The effect of cimetidine on gastric acid, pepsin, and intrinsic factor secretion was assessed in normal male subjects. Cimetidine (300 mg) completely inhibited acid, pepsin, and intrinsic factor concentration and output stimulated by betazole. In contrast, basal output of pepsin and intrinsic factor was not inhibited. We conclude that H2-receptor antagonists inhibit betazole stimulation of intrinsic factor output in addition to their well-known inhibition of acid secretion.

Adult↗

Colonic basophil hypersensitivity.

Contact hypersensitivity reactions were elicited by intraluminal application of DNCB to the colon of guinea pigs and were found sometimes to contain large infiltrates of basophils. These colonic basophil hypersensitivity reactions were accompanied by systemic sensitization and were not seen in nonspecific colonic inflammatory responses induced by croton oil. The heterogenous immune inflammatory responses induced in the colon by DNCB contact sensitivity may serve as a model for the study of inflammatory bowel disease.

Animals↗

Effect of propranolol on ricinoleic acid- and deoxycholic acid-induced changes of intestinal electrolyte movement and mucosal permeability. Evidence against the importance of altered permeability in the production of fluid and electrolyte accumulation.

Hydroxy fatty acids and bile acids produce both intestinal fluid and electrolyte accumulation and increases in inulin clearance, a parameter of mucosal permeability. The relationship of the changes in mucosal permeability to the production of fluid and electrolyte accumulation is uncertain. These experiments were designed to determine whether the alterations of mucosal permeability produced by ricinoleic acid and deoxycholic acid were related to production of hydroxy fatty acid- and bile acid-induced fluid and electrolyte accumulation in the rat colon. Propranolol (1 mg per 100 g of body weight) administered daily for 3 days inhibited ricinoleic acid- and deoxycholic acid-induced Na and water accumulation. In contrast, propranolol did not affect either the increase in inulin clearance or the decrease in electrical potential difference produced by ricinoleic acid and deoxycholic acid. Further, amphotericin B increased inulin clearance by the colon and also increased water and Na absorption. These studies suggest that changes in mucosal permeability are not primarily responsible for hydroxy fatty acid- and bile acid-induced fluid and Na accumulation.

Amphotericin B↗

Importance of the colon in enteric hyperoxaluria.

To investigate the role of the colon in increased oxalate absorption, we measured urinary oxalate and fecal fat excretion in 26 patients with gastrointestinal disease. Eight patients with steatorrhea of various causes (Crohn's disease [two], chronic pancreatitis [four], jejunoileal bypass [one] and extrahepatic biliary obstruction [one]) had hyperoxaluria (greater than 45 mg per 24 hours). All these patients had intact colons. In contrast, none of five patients with ileostomies and steatorrhea secondary to ileal resection had hyperoxaluria. Absorption of 14C-oxalate was increased in three patients with steatorrhea and intact colons but not in three patients with steatorrhea and an ileostomy. Thus, the colon is both the site of and required for increased oxalate absorption in enteric hyperoxaluria. The lack of a direct relation between fecal fat excretion and urinary oxalate excretion in the patients with hyperoxaluria and steatorrhea suggests that steatorrhea, although important, is not the only determinant in the pathogenesis of hyperoxaluria.

Celiac Disease↗

Inhibition of small-intestinal sugar and amino acid transport by the enterotoxin of Shigella dysenteriae I.

The enterotoxin of Shigella dysenteriae I produces fluid and electrolyte secretion in the rabbit ileum. These present studies were designed to evaluate nonelectrolyte transport in rabbit ileal mucosa exposed to Shigella enterotoxin. Both 10 mM galactose and 5 mM L-alanine absorptions were significantly impaired in enterotoxin-exposed ileal mucosa compared with control mucosa. L-Alanine influx was not imparied in two other secretory processes: that induced by cholera enterotoxin and hyperosmolarity. These studies provide evidence that both surgar and amino acid absorptions are diminished in the small intestine by the enterotoxin of S. dysenteriae I.

Alanine↗

Effect of enterotoxins of Vibrio cholerae, Escherichia coli, and Shigella dysenteriae type 1 on fluid and electrolyte transport in the colon.

Experiments were designed to determine whether the enterotoxins of Vibrio cholerae, Escherichia coli, and Shigella dysenteriae type 1 alter the movement of fluid and electrolytes in the rat cecum. Net secretion of water and sodium were observed after incubation of 1.67 X10(-5) mug of purified cholera toxin (choleragen)/ml for 18 hr or of 50 mug/ml for 3 hr. The effect of choleragen on cecal transport of water and electrolytes was related to the dose. In addition, choleragen increased cecal mucosal content of adenosine 3':5'-cyclic phosphate but did not alter the histology of the cecum. The results demonstrate that the colon responds to choleragen in a manner similar to that of other tissues. In contrast, the enterotoxins of both E. coli and S. dysenteriae type 1 failed to affect cecal transport of water and electrolytes. These observations may explain several phenomena associated with the diarrhea produced by bacterial enterotoxins.

Animals↗

Potassium secretion by colonic mucosal cells after potassium adaptation.

Recent studies have demonstrated that chronic potassium loading increases Na-K-ATPase specific activity in kidney tissue and suggest that this enzyme plays a role in renal potassium adaptation. Studies of fluid and electrolyte movement, potential difference (PD), AND Na-K-ATPase were performed in colon and jejunum of the rat in order to further characterize the relationship of Na-K-ATPase to potassium secretion. Experimental rats fed 2.6 meq K/gm diet for 7 days were compared to a control group fed 0.13 meq K/gm. In the colon, chronic potassium loading increased potassium secretion from 0.8 +/- 0.2 to 3.9 +/- 0.9 mueq/min per g tissue (P less than 0.01) and PD from 27 +/- 5.0 to 54 +/- 2.6 mV (P less than 0.001), lumen negative, as Na-K-ATPase increased from 5.0 +/- 0.5 to 11.4 +/- 1.0 muM Pi/mg protein per h (P less than 0.001). In contrast, there was no change in PD, potassium movement, or Na-K-ATPase in the jejunum of potassium-loaded rats. Colonic movement of water, sodium, and chloride was similar in the control and potassium-loaded rats. These results indicate that increased Na-K-ATPase is associated with both increased PD and increased potassium secretion in the colon and provide additional evidence suggesting that Na-K-ATPase may be important in the control of transepithelial potassium movement.

Action Potentials↗