Subdiaphragmatic vagotomy does not block intraperitoneal lipopolysaccharide-induced fever.
Level 5 - mechanism / opinion, no new human data
Animal research (Sprague-Dawley rats)
PubMed 11189031 · doi:10.1016/S1566-0702(00)00224-1
What was done
Male Sprague-Dawley rats underwent either subdiaphragmatic vagotomy or sham surgery. Rats received an intraperitoneal (i.p.) vehicle injection (saline) on a control day followed by i.p. lipopolysaccharide (LPS; 1, 10, or 50 microg/kg) on the experimental day. Core body temperature was monitored by telemetry for 6 hours post-injection. Rats were then sacrificed, and serum, liver, and pituitary samples were collected to measure interleukin-1beta (IL-1beta) levels.
What was found
The abstract reports no numerical values. Intraperitoneal LPS increased core body temperature in both sham-operated and vagotomized rats relative to saline injection. LPS also significantly increased IL-1beta levels in serum, liver, and pituitary compared to controls. There were no significant differences in the magnitude of fever or IL-1beta levels across the tested tissues between sham-operated and vagotomized rats at any tested dose (1, 10, or 50 microg/kg).
Why it matters
These findings demonstrate that subdiaphragmatic vagal afferents are not necessary for mediating fever or peripheral/pituitary IL-1beta induction following intraperitoneal LPS at the doses examined.
Limits
This is an animal study using male rats, limiting direct applicability to human physiology. Sample sizes, exact temperature measurements, and quantitative IL-1beta concentrations are not reported in the abstract. Lower doses of LPS and time points beyond 6 hours were not evaluated.
Cited by
- context Experimental injection of lipopolysaccharide (LPS) into the gut induces a fever response that is abolished if the vagus nerve is transected.