title: On the genesis of gastric haemorrhage.
abstract: An hypothesis involving a three step mechanism to account for the initiation of gastric lesions is described. The mechanism necessitates: (a) A drop in the internal energy (ATP) of the mucosal cells of the stomach upon being subjected to stress; either pathological or psychological. (b) Membranes of mucosal "suicidal sacs" containing potent lysosomal acid-hydrolases are rendered fragile and burst, thus releasing hydrolytic acid-hydrolases into the cytoplasm of the mucosal cells as the latter develop an energy deficit under stress. (c) Gastric mucosal cell necrosis, via the degradation of cytoplasmic and mucinous gastric glycoproteins by these lysosomal acid- hydrolases and subjection of the submucosal tissue to the corrosive effects of the luminal fluid containing hydrochloric acid and pepsin, i.e., initiation of gastric haemorrhage. The above mechanism is a general one that describes events associated with the development of gastric lesions regardless of the factor(s) or the agent(s) initiating gastric mucosal haemorrhage.
authors: Max-Planck Institut fur Biochemie, Martinsried bei Munchen, West Germany.
authors: F M
authors: FM
authors: Fouad
authors: W D
authors: WD
authors: Marshall
authors: P G
authors: PG
authors: Farrell
mesh_terms: D000818:Animals; D004734:Energy Metabolism; D005753:Gastric Mucosa / Q000201:enzymology* / Q000473:pathology; D006471:Gastrointestinal Hemorrhage / Q000201:enzymology / Q000209:etiology* / Q000473:pathology; D006801:Humans; D006867:Hydrolases / Q000378:metabolism; D008247:Lysosomes / Q000378:metabolism / Q000473:pathology*; D008562:Membrane Glycoproteins / Q000378:metabolism*; D009336:Necrosis; D010437:Peptic Ulcer / Q000201:enzymology / Q000209:etiology / Q000473:pathology; D013315:Stress, Psychological / Q000150:complications
chemical_list: D008562:Membrane Glycoproteins; D006867:Hydrolases