Impairment of gastric mucosal defenses measured in vivo in cirrhotic rats

Authors

  • Yasuhiro Nishizaki,

    1. Medical, Veterans Affairs Medical Center of West Los Angeles
    2. Research Services, Veterans Affairs Medical Center of West Los Angeles
    3. Center for Ulcer Research and Education, Department of Medicine, University of California, Los Angeles, Los Angeles, California 90073
    4. Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160, Japan
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  • Jonathan D. Kaunitz M.D.,

    Corresponding author
    1. Medical, Veterans Affairs Medical Center of West Los Angeles
    2. Research Services, Veterans Affairs Medical Center of West Los Angeles
    3. Center for Ulcer Research and Education, Department of Medicine, University of California, Los Angeles, Los Angeles, California 90073
    • CURE Building 115, Rm 219, Wadsworth VAMC, Los Angeles, CA 90073
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  • Masaya Oda,

    1. Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160, Japan
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  • Paul H. Guth

    1. Medical, Veterans Affairs Medical Center of West Los Angeles
    2. Research Services, Veterans Affairs Medical Center of West Los Angeles
    3. Center for Ulcer Research and Education, Department of Medicine, University of California, Los Angeles, Los Angeles, California 90073
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Abstract

Patients with cirrhosis have an increased incidence of gastric ulcers and erosions. We evaluated the effect of carbon tetrachloride—induced cirrhosis on rat gastric mucosal defense mechanisms using our recently developed in vivo fluorescence microscopy technique. Cirrhotic rats had increased portal vein pressure, increased serum aminotransferase concentrations and decreased serum albumin concentrations. We noted significantly more spontaneous gross gastric lesions in the cirrhotic rats. In vivo microscopic measurements revealed that cirrhotic rats had (a) a significantly thinner gastric mucous gel layer, (b) a much greater decrease in surface mucosal cell intracellular pH in response to an acid load, (c) decreased gastric mucosal blood flow and (d) decreased surface cell viability. We conclude that spontaneous gastric mucosal lesions in cirrhotic rats may be related to more rapid penetration of acid through a thinner gastric mucous gel layer and a lower mucosal blood flow. These changes are associated with a decreased ability of the surface cells to maintain intracellular pH homeostasis, increased initial gastric surface cell acidification, decreased surface cell viability and a lower blood flow that probably is inadequate to remove the increased acid. (Hepatology 1994;20:445-452.)

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