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 h
ad increased portal vein pressure, increased serum aminotransferase co
ncentrations and decreased serum albumin concentrations. We noted sign
ificantly 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 a
cid load, (c) decreased gastric mucosal blood how and (d) decreased su
rface cell viability. We conclude that spontaneous gastric mucosal les
ions in cirrhotic rats may be related to more rapid penetration of aci
d through a thinner gastric mucous gel layer and a lower mucosal blood
flow. These changes are associated with a decreased ability of the su
rface cells to maintain intracellular pH homeostasis, increased initia
l gastric surface cell acidification, decreased surface cell viability
and a lower blood flow that probably is inadequate to remove the incr
eased acid.