Inflammatory conditions of the gastrointestinal tract and iron-deficiency a
nemia are very common in humans. Acute intestinal inflammation was patholog
ically established in rats by intraluminal administration of acetic acid in
to the duodenum and the proximal jejunum. The study included two control gr
oups of intact (untreated) rats and sham-operated (saline-treated) rats for
each intestinal segment. A third group of rats received acetic acid. The a
cetic acid-induced inflammatory process was established histopathologically
and biochemically. Two days after treatment, iron absorption was measured
using ligated 10-cm loops of proximal jejunum or ligated duodenum in which
Fe-59 was injected intraluminally (n = 6 in each group). In another four co
ntrol groups (intact and sham-operated for each intestinal segment) and two
acetic acid-treated groups, serosal-luminal secretion of Fe-59 was measure
d after intravenous injection (n = 5 in each group). Fe-59 transfer from th
e lumens of the duodenum and jejunum to the portal system was significantly
lower in those rats in whom inflammation was induced by acetic acid. There
was no apparent serosal-luminal secretion of intravenously injected Fe-59
in any of the studied groups. We conclude that acetic acid-induced intestin
al inflammation significantly reduces iron absorption by the duodenum and t
he proximal jejunum.