Copyright © 1994 Hindawi Publishing Corporation. This is an open access article distributed under the
Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
The basis for the high incidence of infectious complications in portal hypertension (PHT)
remains unclear. The hypothesis that PHT induces bacterial translocation (BT) was tested in
a rat model with or without mono-association with streptomycin resistant Escherichia coli C25
and with or without hypovolemic shock. PHT was achieved by partial portal vein ligation and
three weeks later hypovolemic shock (HS) was induced. Blood, liver, spleen and mesenteric
lymph nodes cultures were performed twenty-four hours later.
PHT promoted BT to mesenteric lymph nodes in indigenous flora (4/6 [67%]) and mono-associated
animals (7/9 [78%]) compared to sham laparotomy and sham shock (SL + SS)
animals (0/6 [0%] and 2/9 [22%] respectively) (p = 0.03). The combination of PHT and HS
resulted in increased mortality in mono-associated (7/15 [47%]) and non mono-associated
animals (8/15 [53%]). No significant translocation was noted in liver and spleen and bacteremia
was found only in the PHT + HS mono-associated animals (4/8 [50%]).
PHT induces BT to mesenteric lymph nodes and this may account for the high incidence of
septic complications associated witti PHT. In this model, the addition of HS to PHT leads to an
increased mortality but without uniform translocation of the gut flora beyond mesenteric lymph
nodes.