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Increased gut permeability to FITC-dextran 70,000, induced by TPN, is reversed by parenteral ampicillin treatment

Purandare, S. ; Offenbartl, K. ; Westrom, B. LU and Bengmark, S. LU (1990) In Surgical Research Communications 8(1). p.7-12
Abstract

Previous experiments by our group have demonstrated that total parenteral nutrition (TPN) in rats increases the gut permeability to FITC-dextran 70,000 when compared to normally fed controls. TPN may thus, by inducing a 'leaky' gut be one co-factor behind the development of 'gut origin sepsis', a recent hypothesis for the development of multiple organ failure (MOF) in patients subjected to severe trauma or complicated surgical disease. Another co-factor behind the development of a damaged gut mucosal barrier under such conditions is a decreased 'colonization resistance' of the gut versus colonization with nosocomial microbial pathogens, a process known to be enhanced by the use of broad-spectrum antibiotics. We therefore studied the... (More)

Previous experiments by our group have demonstrated that total parenteral nutrition (TPN) in rats increases the gut permeability to FITC-dextran 70,000 when compared to normally fed controls. TPN may thus, by inducing a 'leaky' gut be one co-factor behind the development of 'gut origin sepsis', a recent hypothesis for the development of multiple organ failure (MOF) in patients subjected to severe trauma or complicated surgical disease. Another co-factor behind the development of a damaged gut mucosal barrier under such conditions is a decreased 'colonization resistance' of the gut versus colonization with nosocomial microbial pathogens, a process known to be enhanced by the use of broad-spectrum antibiotics. We therefore studied the influence of intravenously administered ampicillin on the gut permeability to FITC-dextran 70,000 after 5 days of TPN in rats and found, quite contrary to our expectations, that ampicillin normalized the TPN-induced increased permeability and that no difference could be demonstrated between normally fed rats and TPN-rats given ampicillin, whereas TPN alone significantly increased the absorption of FITC-dextran into the systemic circulation. This finding points at a role for the intestinal flora at the mucosal level in the pathogenesis of the 'leaky' of TPN and may further have an important implication on the interpretation of TPN-experiments in rats in regard to the situation in humans.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
ampicillin, FITC-dextran, gut permeability, TPN
in
Surgical Research Communications
volume
8
issue
1
pages
6 pages
publisher
M. Gordan and Breach - Harwood Academic
external identifiers
  • scopus:0025328830
ISSN
0882-9233
language
English
LU publication?
yes
id
d47d4a1f-b36e-4f79-87f7-66177718bddd
date added to LUP
2024-12-05 15:30:10
date last changed
2025-04-04 15:01:21
@article{d47d4a1f-b36e-4f79-87f7-66177718bddd,
  abstract     = {{<p>Previous experiments by our group have demonstrated that total parenteral nutrition (TPN) in rats increases the gut permeability to FITC-dextran 70,000 when compared to normally fed controls. TPN may thus, by inducing a 'leaky' gut be one co-factor behind the development of 'gut origin sepsis', a recent hypothesis for the development of multiple organ failure (MOF) in patients subjected to severe trauma or complicated surgical disease. Another co-factor behind the development of a damaged gut mucosal barrier under such conditions is a decreased 'colonization resistance' of the gut versus colonization with nosocomial microbial pathogens, a process known to be enhanced by the use of broad-spectrum antibiotics. We therefore studied the influence of intravenously administered ampicillin on the gut permeability to FITC-dextran 70,000 after 5 days of TPN in rats and found, quite contrary to our expectations, that ampicillin normalized the TPN-induced increased permeability and that no difference could be demonstrated between normally fed rats and TPN-rats given ampicillin, whereas TPN alone significantly increased the absorption of FITC-dextran into the systemic circulation. This finding points at a role for the intestinal flora at the mucosal level in the pathogenesis of the 'leaky' of TPN and may further have an important implication on the interpretation of TPN-experiments in rats in regard to the situation in humans.</p>}},
  author       = {{Purandare, S. and Offenbartl, K. and Westrom, B. and Bengmark, S.}},
  issn         = {{0882-9233}},
  keywords     = {{ampicillin; FITC-dextran; gut permeability; TPN}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{7--12}},
  publisher    = {{M. Gordan and Breach - Harwood Academic}},
  series       = {{Surgical Research Communications}},
  title        = {{Increased gut permeability to FITC-dextran 70,000, induced by TPN, is reversed by parenteral ampicillin treatment}},
  volume       = {{8}},
  year         = {{1990}},
}