glycogen and Peptic-Ulcer

Acute gastric erosions following hemorrhagic shock (stress ulceration) have been attributed to gastric hyperacidity, altered gastric secretion of mucus and an abnormal permeability of the gastric mucosa to H(+). This report aims at presenting evidence supporting an alternate hypothesis: the event linking shock-induced gastric mucosal ischemia to mucosal necrosis is a deficit in gastric mucosal energy metabolism. Our experimental procedure consisted of harvesting the stomachs of rats and rabbits by "stop-freeze" (liquid N(2)) at different intervals after the induction of hemorrhagic shock. Levels of adenosine-phosphates and of glycolytic intermediates in gastric mucosa were measured. We studied the changes in the levels of these substrates produced by shock as well as by factors capable, when combined with shock, of rendering the gastric mucosa more vulnerable to stress ulceration. The influence of shock and of these modifying factors were evaluated by comparison with data from appropriately designed control experiments. In parallel experiments we examined the frequency of stress ulceration (gross and microscopic) under these same standard conditions. There have emerged from these studies a number of observations all based upon data with the highest statistical significance. The data are consonant with the hypothesis stated above: an energy deficit severe enough to cause cellular necrosis is the event linking shock-induced gastric mucosal ischemia and stress ulceration.

Topics: Adenine Nucleotides; Adenosine Triphosphatases; Animals; Energy Metabolism; Fasting; Gastric Mucosa; Glucosephosphates; Glycogen; Ischemia; Lactates; Liver; Male; Muscles; Peptic Ulcer; Phosphocreatine; Pyruvates; Rabbits; Rats; Shock, Hemorrhagic; Taurocholic Acid

The significance of mucous change in the human duodenum in a series of patients with peptic ulcer disease has been appraised. No specific correlation was demonstrated with the acid output of the stomach if the extent of the change is considered, but it was shown to be more common in the higher acid states. Electron microscopic studies confirmed the specific structure of the mucous cells of the duodenum and suggest that they arise either by transformation of Brunner's gland cells or as a distinctive population in the crypts. It is suggested that the mucous change is a protective mechanism involved in some way as yet unknown with the healing of ulcers.

Topics: Biopsy; Cell Membrane; Cell Nucleus; Cytoplasm; Cytoplasmic Granules; Desmosomes; Duodenum; Endoplasmic Reticulum; Epithelial Cells; Epithelium; Extracellular Space; Gastric Juice; Glycogen; Golgi Apparatus; Humans; Intestinal Mucosa; Microscopy, Electron; Mitochondria; Peptic Ulcer; Pyloric Stenosis; Ribosomes; Stomach Neoplasms; Stomach Ulcer

Topics: Adolescent; Biomedical Research; Cholelithiasis; Cholesterol; Gallstones; Gastrectomy; Glycerides; Glycogen; Lipid Metabolism; Lipids; Liver; Nitrogen; Peptic Ulcer; Phospholipids

Topics: Blood; Blood Glucose; Gastrectomy; Glycogen; Humans; Lactic Acid; Peptic Ulcer