Abstract
Artz and Fitts1 reviewed the present state of knowledge about the pathogenesis of gastrointestinal ulcerations associated with lesions of the central nervous system and with burns. They concluded that “It would seem that at the present time, despite intensive investigation over many years, the exact method by which a cutaneous burn induces gastrointestinal lesions is unknown”. There are, however, a number of theories about the mechanism(s) responsible for upper gastrointestinal ulceration and bleeding after burns2–4. The present communication deals with some questions related to the still unresolved problem of the importance of microbial factors and of infection and sepsis1–3,5,6 to the development of gastric ulcers after burns. In the course of studying experimental dorsal burns in germfree and “conventionalized” (multicontaminated ex-germfree) mice, we have discovered that germfree mice develop gastric lesions soon after scalding and that the incidence of these lesions is similar to that in their conventional counterparts.
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References
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EINHEBER, A., WREN, R., PORRO, R. et al. “Curling's Ulcer” in the Germfree Mouse. Nature 214, 298–299 (1967). https://doi.org/10.1038/214298a0
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DOI: https://doi.org/10.1038/214298a0
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