Mechanism of stress ulcer: influence of sodium taurocholate on gastric mucosal energy metabolism during hemorrhagic shock and on mitochondrial respiration and ATPase in gastric mucosa.
In previous reports from this laboratory, we have proposed that stress ulceration complicating hemorrhagic shock results from a gastric mucosal energy deficit due to shock-induced mucosal ischemia. We reasoned that if this hypothesis were correct, an agency known to augment the severity of stress ulceration would be expected to have an adverse effect on gastric mucosal energy metabolism. Others have shown that the severity of stress ulceration developing in animals subjected to hemorrhagic shock is increased by introducing bile salts into the stomach; conversely, the development of stress ulceration can be prevented by ligation of the pylorus or of the common bile duct. We have studied the influence of sodium tauurocholate on the respiration of gastric mucosal mitochondria and on gastric mucosal ATPase. We have also evaluated the influence of the intragastric introduction of taurocholate on the mucosal energy depletion produced by shock. The data presented in this report indicate that taurocholate uncouples oxidative phosphorylation of gastric mucosal mitochondria and inhibits gastric mucosal ATPase. The shock-induced gastric mucosal energy deficit was significantly more severe in the presence of added intragastric taurocholate.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D005753:Gastric Mucosa / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D011817:Rabbits; D012771:Shock, Hemorrhagic / Q000378:metabolism*; D013276:Stomach Ulcer / Q000503:physiopathology*; D013312:Stress, Physiological / Q000503:physiopathology*; D013656:Taurocholic Acid / Q000378:metabolism / Q000494:pharmacology*
D013656:Taurocholic Acid; D000251:Adenosine Triphosphatases