Related Experiment Video
Updated: Apr 6, 2026
07:48
Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation
Published on: May 16, 2016
12.2K
EFFECTS OF EXPERIMENTAL HUMAN ENDOTOXEMIA ON DIAPHRAGM FUNCTION
Jonne Doorduin1, Jenneke Leentjens, Matthijs Kox
1*Departments of Critical Care Medicine †Pulmonary Diseases, Radboud University Medical Center, Nijmegen, The Netherlands.
Shock (Augusta, Ga.)
|July 22, 2015
Summary
Systemic inflammation can augment human diaphragm contractility, contrary to animal models. This study observed increased diaphragm force after endotoxin administration in healthy volunteers.
Area of Science:
- Physiology
- Immunology
- Respiratory Medicine
Background:
- Systemic inflammation is a known risk factor for respiratory muscle weakness.
- Animal models show endotoxin administration causes diaphragm dysfunction.
- Human in vivo effects of endotoxin on diaphragm function remain unstudied.
Purpose of the Study:
- To evaluate diaphragm function in healthy subjects during a model of systemic inflammation.
- To investigate the in vivo effects of endotoxin on human diaphragm contractility.
Main Methods:
- Healthy male volunteers received intravenous lipopolysaccharide (LPS) from E. coli.
- Diaphragm contractility was measured via twitch transdiaphragmatic pressure (Pditw) and compound muscle action potential (CMAPdi).
- Cytokine levels, hemodynamics, respiratory rate, blood gases, and catecholamines were monitored.
Main Results:
- LPS induced flu-like symptoms, hemodynamic changes, and elevated cytokines.
- Diaphragm contractility (Pditw) increased significantly in the early phase post-LPS.
- A trend towards decreased CMAPdi was observed; respiratory rate increased, and PaCO2 decreased.
Conclusions:
- In contrast to animal models, human diaphragm contractility is augmented early after low-dose endotoxin administration.
- This suggests a different inflammatory response in human diaphragm function compared to animal models.
