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Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation
Published on: May 16, 2016
Decreased physiologic variability as a generalized response to human endotoxemia.
Athos J Rassias1, Peter T Holzberger, Alice L Givan
1Department of Anesthesiology, Dartmouth Medical School, Hanover, NH, USA.
Critical Care Medicine
|March 9, 2005
Summary
Transient systemic inflammation, induced by endotoxemia, significantly reduced physiological variability in healthy volunteers. This indicates a generalized increase in the regularity of organ functions during inflammatory responses.
Area of Science:
- Physiology
- Immunology
- Systems Biology
Background:
- Understanding the human body's response to inflammation is crucial for critical care.
- Physiological variability reflects complex system dynamics and health status.
Purpose of the Study:
- To investigate how transient systemic inflammation affects the variability of diverse physiological measures.
- To determine if systemic inflammation alters the time-series behavior of inflammatory response indicators.
Main Methods:
- Prospective study with eight healthy volunteers serving as their own controls.
- Intervention involved intravenous Escherichia coli endotoxin administration on a treatment day.
- Physiological data (heart rate, neutrophil function, cortisol) were collected via continuous ECG and serial blood sampling.
Main Results:
- Time-series data for heart rate (R-R intervals), neutrophil phagocytosis, and plasma cortisol were analyzed.
- Approximate entropy analysis revealed a significant decrease in variability for all measured parameters.
- This indicates an increase in the regularity of these physiological functions during endotoxemia.
Conclusions:
- Systemic inflammation leads to a generalized increase in physiological regularity across divergent organ systems.
- Decreased variability in organ function is a hallmark response to endotoxemia in humans.
- These findings highlight the systemic impact of inflammation on physiological control mechanisms.
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