The vagus nerve in the thermoregulatory response to systemic inflammation.
Level 5 - mechanism / opinion, no new human data
Preclinical animal laboratory study
PubMed 9249579 · doi:10.1152/ajpregu.1997.273.1.R407
What was done
Adult Wistar rats underwent subdiaphragmatic vagotomy or sham surgery with intravenous catheter implantation. On day 28 post-surgery, thermal responses (colonic temperature) to intravenous Escherichia coli lipopolysaccharide (LPS; 0, 1, 10, 100, or 1,000 µg/kg) were measured in either a neutral (30°C) or slightly cool (25°C) environment.
What was found
At 30°C, 1 µg/kg LPS produced a monophasic fever with a maximal colonic temperature rise of approximately 0.6°C in sham-operated rats, which was abated (no temperature change) in vagotomized rats. Doses from 10 to 1,000 µg/kg at 30°C caused biphasic fevers that were not altered by vagotomy. At 25°C, 1,000 µg/kg LPS induced hypothermia of -0.5 ± 0.1°C in sham controls, which was exaggerated to -1.1 ± 0.1°C in vagotomized rats.
Why it matters
The findings show that vagal afferents mediate the febrile response to low levels of systemic pyrogens, whereas higher pyrogen doses activate non-vagal pathways.
Limits
The abstract does not report sample sizes. The study is restricted to adult rats, and the mechanisms underlying the exaggerated hypothermic response to high-dose LPS in cool conditions were not elucidated.
Cited by
- context Experimental injection of lipopolysaccharide (LPS) into the gut induces a fever response that is abolished if the vagus nerve is transected.