sodium-taurodeoxycholate and Stomach-Ulcer

Since chronic gastritis is adversely affected by reflux bile acids, we are interested in which of these bile acids cause the most damage to the gastric mucosa as ulcerogenic factors in the stomach. We examined 34 patients suffering from the peptic ulcers, and have assumed that taurine conjugated deoxycholic acid (TDC) and chenodeoxycholic acid (TCDC) may act as the mst ulcerogenic factors. Moreover TCDC was suggested to be associated with the cystic dilatation of the gastric gland. It was also suggested that TDC is involved in the increased frequency of intestinal metaplasia as a factor backgrounding cancer.

Topics: Adult; Aged; Atrophy; Bile Reflux; Chenodeoxycholic Acid; Dilatation, Pathologic; Gastric Mucosa; Humans; Middle Aged; Stomach Ulcer; Taurodeoxycholic Acid

Although recent clinical reports suggest that greater than normal amounts of dihydroxy secondary bile acids appear in the gastric content of patients with postoperative alkaline reflux gastritis, the pathophysiologic significance of these observations is unclear. We addressed this problem by usiong chambered ex vivo wedges of proximal canine gastric wall. The effects of 1 and 2 mM concentrations of the dihydroxy secondary bile acid, taurodeoxycholic, were compared with those of its parent trihydroxy primary bile acid, taurocholic. The parameters of mucosal function evaluated included the net flux of hydrogen ion, the transmural electrical potential difference, mucosal blood flow determined by radiolabeled microsphere embolization, and the severity of mucosal damage induced in mucosa rendered ischemic by wedge-specific intra-arterial low-dose vasopressin infusin. The results indicate that at each concentration in both ischemic and nonischemic mucosa the dihydroxy secondary bile acid induced a greater depression in potential difference, a more profound increase in mucosal permeability to hydrogen ion, and in ischemic mucosa a more severe degree of gross mucosal damage than did the trihydroxy primary bile acid. These effects may be related to a greater lipid solubility and consequent capacity to disrupt cell membranes.

Topics: Animals; Deoxycholic Acid; Dogs; Female; Gastric Mucosa; Ischemia; Male; Stomach Ulcer; Taurocholic Acid; Taurodeoxycholic Acid

Topics: Animals; Deoxycholic Acid; Dogs; Gastric Mucosa; Stomach Ulcer; Taurocholic Acid; Taurodeoxycholic Acid

Reflux of duodenal contents into the stomach has been implicated in the disruption of mucosal defence and the subsequent occurrence of gastric ulcer. The change produced in the rheological properties following the addition of bile salts and phospholipids to mucus samples was used to assess resultant structural changes. Sodium deoxycholate, sodium taurodeoxycholate, sodium glycocholate, and lysophosphatidylcholine decreased both viscosity and elasticity, indicating that structural breakdown had occurred, whereas phosphatidylcholine could not be shown to have any effect. It is therefore suggested that some of the ulcerogenic activity of naturally occurring surfactants may be associated with their ability directly to reduce mucus consistency.

Topics: Bile Acids and Salts; Compliance; Deoxycholic Acid; Glycocholic Acid; Humans; Mucus; Phosphatidylcholines; Sodium Dodecyl Sulfate; Stomach Ulcer; Taurodeoxycholic Acid; Viscosity