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Updated: Jul 16, 2026
06:43
Functional Assessment of Intestinal Tight Junction Barrier and Ion Permeability in Native Tissue by Ussing Chamber Technique
Published on: May 26, 2021
Intestinal paracellular permeability is not affected in chronic congestive heart failure
M Schaufelberger1, I Ekman, E Björnsson
1Department of Internal Medicine, Sahlgrenska University Hospital Ostra, Gothenburg, Sweden. maria.schaufelberger@hjl.gu.se
European Journal of Heart Failure
|March 27, 2007
Summary
This study found no evidence of a dysfunctional gastrointestinal barrier in chronic heart failure (CHF) patients. The (51)Cr-EDTA test did not detect increased intestinal permeability or endotoxin translocation in CHF.
Area of Science:
- Cardiology
- Gastroenterology
- Immunology
Background:
- Chronic heart failure (CHF) may involve gastrointestinal (GI) barrier dysfunction.
- Endotoxin translocation from the gut could trigger systemic inflammation, impacting cardiac function.
- Cytokine elevation in CHF is a known concern, potentially linked to gut permeability.
Purpose of the Study:
- To investigate GI barrier function in stable CHF patients.
- To determine if endotoxin is detectable in the venous blood of CHF patients.
- To explore the relationship between GI permeability and cardiac function.
Main Methods:
- Nineteen stable CHF patients (NYHA II-III) were studied.
- Gastrointestinal permeability assessed using the (51)Cr-EDTA absorption test.
- Healthy subjects and bone marrow transplant patients served as controls.
Main Results:
- No significant difference in intestinal permeability was observed between CHF patients and control groups.
- Peripheral oedema status did not correlate with GI permeability.
- Endotoxins were below the detection limit in all investigated CHF patients.
Conclusions:
- The (51)Cr-EDTA absorption test does not support a dysfunctional GI barrier in CHF patients.
- The hypothesis linking GI barrier dysfunction to endotoxin translocation in CHF is not supported by this study.
- Further research may be needed to explore alternative mechanisms of inflammation in CHF.
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